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The gut microbiota exerts profound influence on poultry immunity and metabolism through mechanisms that yet need to be elucidated
Here we used conventional and germ-free chickens to explore the influence of the gut microbiota on transcriptomic and metabolic signatures along the gut-lung axis in poultry
Our results demonstrated a differential regulation of certain metabolites and genes associated with innate immunity and metabolism in peripheral tissues of germ-free birds
we evidenced the gut microbiota’s capacity to regulate mucosal immunity in the chicken lung during avian influenza virus infection
by fine-analysing the antiviral pathways triggered by the short-chain fatty acid (SCFA) butyrate in chicken respiratory epithelial cells
we found that it regulates interferon-stimulated genes (ISGs)
These findings emphasize the pivotal role of the gut microbiota and its metabolites in shaping homeostasis and immunity in poultry
offering crucial insights into the mechanisms governing the communication between the gut and lungs in birds
the regulation of microbiota composition has well-recognised consequences for immune development and overall health in humans and mammalian model species
Understanding the mechanisms through which the GM and SCFAs influence metabolism and immunity in the respiratory tract and other peripheral tissues is an area of active research and would allow the development of probiotics/postbiotics with optimised capacity to enhance immune system functions beyond the gut
the gut-lung axis in birds is largely unexplored
despite most pathogens in commercial poultry targeting the gut and/or airways
To define how the chicken GM regulates metabolism and immunity in the gastrointestinal tract and in the periphery
we analysed transcriptomic and metabolic signatures in conventional (CV) and germ-free (GF) chickens
GF birds exhibited significant physiological changes in the caecal compartment
lacking central GM-derived metabolites like SCFAs
SCFA detection in peripheral compartments of CV birds and differential expression of innate immunity genes in GF birds’ peripheral tissues further corroborated the functional existence of a gut-lung axis in birds
GF chickens showed different immunoregulatory responses to infection
displayed antiviral effects in chicken respiratory epithelial cells
likely via the regulation of interferon-stimulated genes
The observed antiviral signalling mechanism would involve HDAC inhibition and Sp1-dependent regulation of the OASL promoter
shedding light on new mechanisms through which the GM regulates poultry mucosal immunity along the gut-lung axis in the chicken
Perturbations in the growth media were visually examined after 18 hours of incubation
a drop from the BHI fecal-broth media was placed on a glass slide and examined under a microscope (×40 magnification) for the presence or absence of bacteria
If suspicion arose regarding the presence of these microorganisms
a sample from the BHI culture was inoculated onto BHI agar plates and incubated at 37 °C for 18 to 48 hours for further analysis
Swabs from isolators were periodically tested during hatching and post-hatching periods until the end of the experiment
employing the same detection methods for bacteria and fungi described above
All experiments were conducted in compliance with the relevant European and national regulations and authorised by the local ethics committee (Comité d’Ethique en Expérimentation Animale Val de Loire) under the reference number APAFIS#30655-2021042114338110 v1
CV and GF birds (n = 8 per group) were sacrificed by cervical dislocation followed by blood withdrawal from the occipital venous plexus
Blood samples were stored in heparin-coated tubes for subsequent plasma preparation
and lungs were immediately collected from each chicken
and stored at −80 °C until further use for metabolomics analysis and/or RNA and DNA extraction and sequencing
a group of 24 GF and 24 CV birds were equally inoculated intra-tracheally (i.t.) with 0.2 ml of 106 EID550 of H7N1
and 15 GF and 15 CV control (mock) birds were inoculated i.t
and plasma were recovered from a group of animals (n = 5–8) for different downstream analyses
Birds were carefully monitored (twice daily) during the course of infection
and diseased birds presenting at least 4 of the following symptoms for 24/48 hours were killed by intravenous pentobarbital injection (humane endpoint): ruffled feathers
Clinical signs were evaluated according to the following score: 0 (no clinical signs)
or 3 (dead or euthanized due to persistent severe clinical signs)
A scoring system was used to evaluate macroscopic lung lesions as follows: 1 (mild
2 (moderate oedema and with haemorrhage and fibrinous exudate over ~1/4 of the lung)
or 3 (severe haemorrhage and extensive oedema over ~1/2 of the lung)
Cells were cultured in Dulbecco’s Modified Eagles’s Medium (DMEM) supplemented with 10% fetal calf serum (FCS) (Gibco
and 100 UI/ml penicillin and 100 μg/ml streptomycin (PS
cells were plated at 5 × 106 cells/ml in 12-well plates
Sigma-Aldrich-UK) at varying concentrations and times
Some experiments included chicken interferon alpha (Yeast-derived
Cell lysates and RNA were analysed for gene expression and metabolomics
Cell viability and counts were assessed using Spark® Cyto (Tecan
Switzerland) after Trypan Blue (Sigma-Aldrich
Primers M52C and M253R span conserved sequences in gene segment 7 of influenza A virus and have no homology to nucleotide sequences from other species available from GenBank
Viral load quantification was expressed as PFU/mL or M1 genomic copy numbers
Cellular RNA extractions from infection experiments with the H1N1 and H7N1 strains were also used for gene expression analysis
UK) was used to measure class I and II HDAC activity in CLEC213 cells according to the manufacture’s protocol
the acetylated peptide substrate was added to the cell culture medium in the presence or absence of butyrate
and peptide cleavage requiring deacetylated protease activity was quantified by measuring the release of luminescent aminoluciferin using a GloMax plate reader (Promega
Reduction in relative light units (RLU) correlated with decreased HDAC activity due to the inhibitory properties of the tested molecule
Trichostatin A served as a positive control
Data are presented as RLU or as percentage of HDAC activity
with untreated cells as the reference (100%)
Caecal contents samples (20–50 mg) were homogenised in 1.2 ml of phosphate buffer (0.2 M
dried using a SpeedVac Vacuum Concentrator
500 µl of supernatant were transferred into 5 mm NMR tubes
and cell lysates were homogenised in 4.85 ml of methanol/water (80/20
2 ml of dichloromethane per gram of tissue were added
2 ml of dichloromethane and 2 ml of water per gram of tissue were added
Samples were dried using a SpeedVac Vacuum Concentrator
reconstituted in 200 µl of phosphate buffer (0.2 M
150 µL of supernatant were transferred into 3 mm NMR tubes
and 50 µL of TSP solution (1 mM) were added to the NMR tube
1H NMR spectra were obtained at 300 K on a Bruker Avance III HD 600 MHz NMR spectrometer
The “noesypr1d” pulse sequence was used for water signal suppression with a mixing time of 100 ms
A total of 1024 and 256 transients were collected for tissue and caecal samples
into 64k data points using a spectral width of 12 ppm
an exponential line broadening function of 0.3 Hz was applied to the FID
All NMR spectra were phase- and baseline-corrected and referenced to the chemical shift of TSP (0 ppm) using Topspin (V3.2
Metabolite concentrations were calculated using the TSP signal at 0 ppm integrating for 9 protons and with known concentrations of different metabolites
with significant logarithmic fold change ratios determined by Wald tests and Benjamini-Hochberg adjustment for multiple testing (P < 0.01)
To distinguish monocytes and macrophages in the spleen
we utilised an APC-conjugated antibody (clone Kul01
IgG1) targeting the chicken mannose receptor C-type 1 like B (MRCL1-B) of avian monocytes and macrophages
we incorporated staining for MHC-II (clone 21-1A6
T lymphocytes were identified based on the expression of their T-cell receptor (TCR) and coreceptors
we employed monoclonal antibodies against CD4 (clone CT-4
Chicken thrombocytes were characterised using antibodies recognising the fibrinogen receptor CD41/61 (clone 11C3
we utilised an APC-conjugated antibody recognising the antigen Bu-1 (clone AV20
Quadrant markers were established based on negative populations and isotype controls
cell viability was assessed using the fluorescent DNA intercalator 7-aminoactinomycin D (7-AAD
Cell acquisition (5 × 105 events) was performed using a BD FACSCanto II cytometer (BD Biosciences)
with subsequent analysis conducted using FlowJo 7.5.3 software (TreeStar Inc.
The percentage of the analysed population relative to total acquired events was employed in graph construction
Unless otherwise specified above or in the figure legends
data are presented as the median or mean ± SEM
The unpaired Student’s t test was employed to compare the means of two independent groups
one-way analysis of variance (ANOVA) was conducted to ascertain statistically significant differences among the means
followed by a Tukey post-hoc test utilising a Studentized range statistic to perform pairwise comparisons between groups
USA) was employed for statistical analysis
Significance levels were set at p < 0.05 for most analyses
these data highlight that the isolators employed in this study did not impede the development of a complex caecal microbiota in our chicken line
log2 fold change ≥1) from RNAseq data from germ-free (GF) chickens
compared to conventionally raised (CV) chickens at 21 days post-hatch were analysed using Ingenuity Analysis Pathway software
visualised as a “bubble chart.” Circles in each row represent groups of genes associated with a biological function
with size indicating gene count and colour reflecting an intensity gradient ranging from overexpression (orange pattern) to downregulation (blue pattern) in GF chickens using CV chickens as the normalisation controls
The software enables tissue or cell selection and provides inferences on unrepresented genes
A confidence-boosting maximum adjusted p value threshold was applied: 0.45 for caeca (a)
including the analyses of the top 244 genes from the caeca RNAseq analyses; 0.4 for lungs (b)
including the analyses of the top 280 genes from the lungs RNAseq analyses; and 0.1 for spleen (c)
including the analyses of the top 84 genes from the spleen RNAseq analyses
lungs or spleen samples from 5 GF chickens or 5 CV chickens (n = 5 biological replicates)
log2 fold change ≥1) associated with immunity and inflammation were identified in the RNAseq analyses of caeca (a)
and spleen (c) samples of 21 days-old chickens
This selection included standout genes coding for transcription factors
enzymes and other molecules with broad functions in innate and adaptive immunity of vertebrates
Histograms present the relative expression of each gene in log2 format for germ-free (GF) animals compared to conventionally raised (CV) animals
A downregulation trend is particularly pronounced in the caeca and moderately in the spleen
contrasting regulatory phenomena with similar intensities coexist
d Certain DEGs identified using RNAseq analyses followed by an assessment through the Ingenuity Analysis Pathway software (in which a confidence-boosting maximum adjusted p value threshold was applied) are shared by the three organs studied
A Venn diagram illustrates DEG counts per organ
reveal OASL as the sole immune-related gene significantly regulated in all three examined organs
these findings highlight the GM’s significant impact on the transcriptional regulation of IFN-related genes along the gut-lung axis in the chicken
remains largely unaffected by the lack of a GM
with resulting p values generating colour scales for the histograms
exclusion threshold) were applied to the presented data
Each group comprised caecal contents or lung samples from 6 GF chickens or 6 CV chickens (n = 6 biological replicates)
Unpaired student’s t test was employed for statistical analyses (a
These observed disparities underscore the GM’s profound influence on chicken metabolism and immune response
providing solid evidence to further explore these regulatory mechanisms in the context of infectious challenges
Germ-free (GF) animals infected via the tracheal route with a 5 × 105 EID50 dose of LPAIV H7N1 exhibited a disease profile indistinguishable from their conventional (CV) counterparts
Macroscopic lung lesion scores (haemorrhage
oedema) (a) and viral genome copies in the lungs (b) or in the caeca (c) at Days 1–3 post-infection (p.i.) show no significant differences between the two groups
d Examination of infection kinetics in GF chickens’ lungs using Medium-Throughput qPCR (Fluidigm) indicates sustained expression of genes associated with inflammation (IL8L1
The heatmap illustrates relative expression levels in GF-infected animals compared to CV-infected animals on the same day
Each group comprised caeca or lungs samples from 5 mock and 8 infected GF chickens or 5 mock and 8 infected CV chickens (n = 5–8 biological replicates)
each biological replicate is the mean of three technical replicates
Statistical analysis employed unpaired student’s t test (a–c) or one-way ANOVA followed by Tukey multiple comparison test (d)
Data are represented as the median (a–c) or the mean ± SEM (d
These genes showed lower expression at 24 and 48 hours compared to CV animals but a significant elevation at 72 hours
indicating a sustained antiviral response beyond 48 hours in GF animals
These changes also influenced mucosal immunity
as seen in the distinct regulation pattern for IL22 and its receptors (IL22RA1
reduced expression of anti-inflammatory genes like TGFB and SOCS3 at 72 hours p.i
in GF animals possibly indicates an unresolved inflammatory state
while the absence of GM does not hinder antiviral responses against AIV in chickens
it influences the quality and amplitude of the immune response at the transcriptional level
The CLEC213 chicken lung epithelial cell line was treated with different concentrations of SCFA for 16 h
and acetate was assessed using a Spark® Cyto and expressed as the percentage of cell viability compared to untreated controls (a)
qPCR analysis demonstrates that acetate (b)
and propionate (d) elicit different responses in terms of selected innate immune gene expression in CLEC213 cells
the induction of OASL by butyrate exhibits a concentration-dependent relationship (e)
Statistical analysis was performed using One-way ANOVA followed by Tukey multiple comparison test
with significance levels indicated as follows: *p < 0.05
in which each biological replicate is the mean of three technical replicates
c–e an n = 5–7 biological replicates is shown
with colour scales in histograms corresponding to p values
c Butyrate induced positive regulation across diverse biological functions in chicken lung epithelial cells
as depicted in a ‘bubble chart’ generated from RNAseq data analysis using Ingenuity Analysis Pathway software
Circles in each row represent groups of genes associated with a biological function
with size indicating gene count and colour reflecting an intensity gradient ranging from overexpression (orange pattern) to downregulation (blue pattern) in butyrate (3 mM) treated cells using untreated cells as the normalisation controls
A confidence-boosting maximum adjusted p value threshold of 045 was applied
d The log2 relative expression of a group of selected immune-related genes extracted from all DEG from RNAseq data (padj < 0.05
log2 fold change ≥1) in cells receiving butyrate (3 mM) compared to untreated cells at 16 h
Data in d are represented as the mean ± SEM
Butyrate also exhibits pro-inflammatory actions
mirroring observations in GF animals (which lack systemic butyrate) and emphasising the role of SCFA in regulating ISGs in the respiratory mucosa
f Identification of potential binding sites for Sp1 in the OASL promoter of selected bird and mammalian species
One-way ANOVA followed by Tukey multiple comparison tests (a–d) was employed for statistical analyses
b an n = 3 biological replicates are shown
Data in e are representative of an n = 6 biological replicates
without affecting vital cellular functions in the CLEC213 cell line
the function of these genes in the chicken are still not resolved
although their conservation among several vertebrate species suggests that they may exhibit overall conserved biological functions
Butyrate treatment (3 mM) improves viral clearance in CLEC213 cells infected with an LPAIV H1N1 avian influenza strain
Incubation with butyrate prior to infection (MOI 0.1 for 6 hours or MOI 0.01 for 16 hours) significantly reduces viral titre (PFU/ml) (a) and genomic copies (b) compared to untreated cells
qPCR analysis showed increased expression of IFNB and OASL in butyrate-treated infected cells (c)
Silencing OASL expression abolishes butyrate’s antiviral effects
resulting in infectious titre identical to untreated cells
concomitantly with reduced OASL expression (d)
b) and One-way ANOVA followed by Tukey multiple comparison test (c
a an n = 3 biological replicates are shown
b–d an n = 3 biological replicates is shown
the overall antiviral effects of butyrate would involve enhanced metabolic activity
regulatory influence on inflammatory signals
suggesting potential compensatory mechanisms for lower nutrient absorption
studies linking the GM and SCFA to the regulation of ISG15 or OASL are currently lacking
OASL’s regulation in GF animals appears markedly altered both at homoeostasis and infection
emphasising its dependence upon positive microbial signals coming from the GM in the chicken
Our comparative study using GF and CV chickens thus provides robust evidence of OASL regulation by the microbiota
shedding new light on evolutionary biology and comparative immunology
its expression decreased by 2 log2 at homoeostasis and surged to a level 60 times higher 24 hours post-infection
it appears that a delay in triggering the antiviral innate response in the lungs of GF chickens does not impair the proper control of viral load compared to CV chickens
the selected innate immune genes in GF chickens are already at a lower basal level than those in CV counterparts
This could potentially attenuate the exacerbated inflammatory response that leads to severe pneumonia and increased mortality
as overall lung pathology and clinical scores are similar between CV and GF chickens
Further studies with a broader analysis beyond day 3 are necessary to determine if GF animals can sustain viral load control and if their innate immune response will peak and resolve similarly to CV animals
This remains undefined at present and could lead to the discovery of new molecular mechanisms through which the chicken GM directs innate immunity toward effective and pro-resolutive viral clearance
potentially mitigating inflammation by preventing HIF activation in pulmonary epithelium
butyrate may regulate OASL expression through additional metabolic pathways yet to be defined
highlighting its dual role in shaping immunity and metabolism in our respiratory epithelial system
This unveils a novel mechanism through which a GM-derived SCFA modulates antiviral immunity in peripheral organs of birds
Further investigation into the multifaceted regulation of the type I IFN response by butyrate and its varying effects on virus infection in vertebrates is warranted
Our research revealed the intricate interaction between caecal microbiota-derived SCFAs
and their role in regulating protective immunity and metabolism across the gut-lung axis in chickens
These insights have broad implications for understanding the gut-lung axis and developing prophylactic strategies in commercial poultry through microbiota modulation
Further exploration of butyrate’s multifaceted effects and its interactions with specific cellular pathways is crucial to harnessing the full potential of SCFAs as next-generation postbiotics for poultry birds
The authors declare that all data supporting the findings in this study are available within the article
or from the corresponding author on reasonable request
All RNAseq data and 16S sequencing data were deposited in the ELIXIR Deposition Database ArrayExpress under the accession numbers E-MTAB-14262
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Shifting the balance: antibiotic effects on host–microbiota mutualism
From dietary fiber to host physiology: short-chain fatty acids as key bacterial metabolites
Butyrate protects mice from clostridium difficile-induced colitis through an HIF-1-dependent mechanism
Microbial regulation of host physiology by short-chain fatty acids
Principles and clinical implications of the brain–gut–enteric microbiota axis
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gut health and chicken productivity: what is the connection
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Modeling immunocompetence development and immunoresponsiveness to challenge in chicks
A novel chicken lung epithelial cell line: characterization and response to low pathogenicity avian influenza virus
interdomain region of the non-structural protein NS1 of an avian H1N1 influenza virus increases its replication and pathogenicity in chickens
Detection of influenza A viruses from different species by PCR amplification of conserved sequences in the matrix gene
The microbial metabolite butyrate regulates intestinal macrophage function via histone deacetylase inhibition
Inhibition of histone deacetylase activity by butyrate
Efficient extraction from mice feces for NMR metabolomics measurements with special emphasis on SCFAs
Stable suppression of gene expression by RNAi in mammalian cells
Role of the chicken oligoadenylate synthase-like gene during in vitro Newcastle disease virus infection
Cutadapt removes adapter sequences from high-throughput sequencing reads
RSEM: accurate transcript quantification from RNA-Seq data with or without a reference genome
Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2
g:Profiler: a web server for functional enrichment analysis and conversions of gene lists (2019 update)
An accurate and efficient experimental approach for characterization of the complex oral microbiota
Swarm: robust and fast clustering method for amplicon-based studies
The SILVA ribosomal RNA gene database project: improved data processing and web-based tools
Characterization of chicken leukocyte subsets from lymphatic tissue by flow cytometry
Untangling the genetic basis of fibrolytic specialization by Lachnospiraceae and Ruminococcaceae in diverse gut communities
Effect of cecal microbiota transplantation between different broiler breeds on the chick flora in the first week of life
Contact with adult hen affects development of caecal microbiota in newly hatched chicks
The effects of secretory IgA in the mucosal immune system
Structure and functions of cellular redox sensor HSCARG/NMRAL1
Amphiregulin promotes intestinal epithelial regeneration: roles of intestinal subepithelial myofibroblasts
Macrophage FABP4 is required for neutrophil recruitment and bacterial clearance in Pseudomonas aeruginosa pneumonia
Visualisation and characterisation of mononuclear phagocytes in the chicken respiratory tract using CSF1R-transgenic chickens
The avian lung-associated immune system: a review
Mzb1 protein regulates calcium homeostasis
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Identification of a novel cytokine-like transcript differentially expressed in avian γδ T cells
Type I interferon (IFN)-regulated activation of canonical and non-canonical signaling pathways
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Butyrate in energy metabolism: there is still more to learn
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Microbiota regulation of viral infections through interferon signaling
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Mimicking the passage of avian influenza viruses through the gastrointestinal tract of chickens
Microbiota regulates immune defense against respiratory tract influenza A virus infection
Gut microbiota modulates type I interferon and antibody-mediated immune responses in chickens infected with influenza virus subtype H9N2
Butyrate reprograms expression of specific interferon-stimulated genes
Inhibition of interferon gamma signaling by the short chain fatty acid butyrate
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Sp1 phosphorylation and its regulation of gene transcription
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We express our gratitude to the staff of the Plate-forme d’Infectiologie Expérimentale (UE PFIE
INRAE) for providing the necessary infrastructure and technical support essential for conducting the animal experiments in this study
France (specifically Santé Animale—SA and Microbiologie et Chaine Alimentaire—MICA divisions)
by “EuroFéRi” (FEDER-FSE Centre Val de Loire 2014-2020
contributed to data acquisition and analysis
provided molecular and bioinformatics tools and participated in data analysis
analysed and interpreted data using bioinformatics
All authors contributed to writing the article and approved the submitted version
The authors declare no competing interests
Communications Biology thanks Mohamed Faizal Abdul-Careem
reviewer(s) for their contribution to the peer review of this work
Primary Handling Editors: Sabina Leanti La Rosa and Tobias Goris
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations
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This article is part of the Research TopicSensing DNA in Antiviral Innate ImmunityView all 14 articles
The anti-viral immune response is dependent on the ability of infected cells to sense foreign nucleic acids
the pattern recognition receptor (PRR) cyclic GMP-AMP synthase (cGAS) senses viral DNA as an essential component of the innate response
cGAS initiates a range of signaling outputs that are dependent on generation of the second messenger cGAMP that binds to the adaptor protein stimulator of interferon genes (STING)
the cGAS/STING pathway is essential not only for the production of type-I interferons in response to intracellular DNA stimulation
but also for regulation of macrophage effector functions including the expression of MHC-II and co-stimulatory molecules
the cGAS/STING pathway was found to be responsible for type-I interferon production and MHC-II transcription
The sensing of fowlpox virus DNA is therefore essential for mounting an anti-viral response in chicken cells and for regulation of a specific set of macrophage effector functions
It is not currently clear in what contexts these disparate signaling outputs are activated by cGAS/STING and to what extent they cross-talk with each other
Like other poxviruses the cytoplasmic replication cycle of FWPV exposes large amounts of foreign DNA to intracellular DNA sensing PRRs
making cGAS a likely candidate for sensing FWPV infection and making FWPV a potentially useful tool for delineating nucleic acid sensing mechanisms in avian systems
The mechanisms by which FWPV is sensed by PRRs during infection have not
In this study we show the existence of a cGAS/STING pathway in chicken macrophages and determine its downstream signaling outputs
Using cGAS and STING CRISPR/Cas9 knockout HD11 cells and pharmacological inhibitors of STING and TBK1 in primary macrophages
we show that the activation of cGAS by intracellular DNA induces an IFN-I response and that this response can be enhanced by priming cells with IFNα
we show that cGAS/STING signaling in macrophages can enhance transcription of specific immune recognition molecules including genes encoding the class II major histocompatibility complex (MHC-II) and co-stimulatory proteins
Using FWPV mutants that are deficient in specific immunomodulators we are able to overcome the immunosuppression of wild type FWPV and show that this virus is sensed by cGAS
resulting in IFN-I and MHC-II transcription
These data show that the cGAS/STING/TBK1 pathway senses viral DNA in chicken macrophages and that this pathway regulates not only the antiviral interferon response but also modulates specific components of macrophage effector function machinery
polyinosinic-polycytidylic acid (poly(I:C)
2’3’-cGAMP (Invivogen) and chicken interferon alpha (Yeast-derived Recombinant Protein
Inc) were diluted in nuclease-free water (Ambion
H-151 and BX795 (Invivogen) were diluted in DMSO
following the manufacturer’s protocols
HD11 cells, an avian myelocytomatosis virus (MC29)-transformed chicken macrophage-like cell line (15)
Germany) complemented with 2.5% volume per volume (v/v) heat-inactivated foetal bovine serum (FBS; Sera Laboratories International Ltd)
2.5% volume per volume (v/v) chicken serum (New Zealand origin
10% Tryptose Phosphate Broth solution (Gibco
50 µg/ml of penicillin/streptomycin (P/S; Gibco
Chicken embryonic fibroblasts (CEFs) (Pirbright Institute
5% CO2 and were grown in Dulbecco’s Modified Eagle Medium (DMEM) -F12 with Glutamax (Gibco)
According to the MB21D1 (cGAS) and TMEM137 (STING) sequences obtained from the Ensembl database (release 94), single guide (sg)RNA sequences (Table 1) were designed targeting the catalytic domain (residues 11-13 and 109) and start of the open reading frame
Genome editing of HD11 was performed using ribonucleoprotein (RNP) delivery. tracrRNA was mixed with the target specific sgRNA (Table 1)
the tracrRNA/sgRNA mix was incubated with the Cas9 protein (IDT
Belgium) and electroporation enhancer at 21°C
The successfully edited populations (using guides cGAS sg3 and STING sg1) were diluted to a concentration of 0.5 cell/well and seeded in 96-well plates
Individual clones were sequenced by MiSeq and the confirmed knockout clones were expanded for experiments
Chicken bone marrow derived macrophages (BMDM) were generated as previously described (17)
femurs and tibias of 4 week-old immunologically mature White Leghorn (PA12 line) outbred chickens were removed
both ends of the bones were cut and the bone marrow was flushed with RPMI supplemented with P/S
Cells were then washed and re-suspended in RPMI
loaded onto an equal volume of Histopaque-1077 (Sigma-Aldrich
Cells at the interface were collected and washed twice in RPMI
were seeded in triplicates at 1×106 cells/ml in sterile 60 mm bacteriological petri dishes in RPMI supplemented with 10% FBS
P/S and 25 ng/ml recombinant chicken colony stimulating factor 1 (CSF-1) (Kingfisher Biotech
Half of the medium was replaced with fresh medium containing CSF-1 at day 3
adherent cells were harvested and cultured in RPMI supplemented with 10% FBS
Procedures were performed in strict compliance with legal dispositions applicable in France
which state that animal euthanasia for the only purpose of organ or tissue use is not considered as an experimental procedure with obligation of submission to ethics committee for approval (Ordinance 2013-118
published in the Journal Officiel de la République Française # 0032 of the February 7
cGAS and STING knockouts) were seeded in 12-well plates at a density of 3×105 cells/well
the cells were transfected using TransIT-LT1 (Mirus Bio
or 5 µg/ml) or Poly(I:C) (1 µg/ml)
and harvested 6 or 16 h post-transfection
IFNα (200 ng/ml) was added 16 h prior to transfection
2’3’ cGAMP was added at a concentration of 2.5 µg/ml and cells were harvested 6 h post-treatment
BMDM were seeded in 6-well plates at 8x105 cells/ml
cells were transfected using TransIT-LT1 with HT-DNA (2 µg/ml)
IFNα (50 ng/ml) was added 16 h prior transfection to the cells supernatants
2’3’ cGAMP was added to cells supernatants at the concentration of 10 µg/ml and the cells were harvested 6 h post-treatment
The presence of IFN-I in supernatants of stimulated BMDM was measured indirectly using a luciferase-based Mx-reporter bioassay (18)
cells from the quail fibroblast cell line CEC32 carrying the luciferase gene under the control of chicken Mx promoter (kindly provided by Prof
Germany) were seeded at 2.5×105 cells/well in 24-well plates and incubated at 41°C under 5% CO2
cells were incubated for 6 h with the diluted supernatants (1/10 of total volume)
Medium was removed and cells were washed twice with PBS
Cells were lysed using the Cell Culture Lysis Reagent (Promega
according to the manufacturer’s instructions
and luciferase activity was measured using the Luciferase assay reagent (Promega
USA) and a GloMax-Multi Detection System (Promega
BMDM or HD11 viability following different stimuli was assessed using the fluorescent DNA intercalator 7-aminoactinomycin D (7-AAD
and the cells were harvested and washed in PBS
Cells were stained according to the manufacturer’s protocol and the viability was analyzed by flow cytometry (BD FACS Calibur)
Data were expressed as the percentage of 7AAD positive cells over total acquired events (50,000 cells)
Cells were lysed by overlaying with 250 µl of lysis buffer containing 4 M guanidine thiocyanate
and the solution was transferred to a silica column (Epoch Life Science
USA) and centrifuged; all centrifugation steps were performed for 90 s at 16,600 g
The bound RNA was washed by centrifugation with 500 µl of buffer containing 1 M guanidine thiocyanate
followed by a double washing step with 500 µl of wash buffer 2 [25 mM Tris pH 7 and 70% (v/v) ethanol]
RNA was eluted by centrifugation in 30 µl of nuclease-free water and the concentration was measured using a NanoDrop 2000 Spectrophotometer (Thermo Scientific
Using 500 ng of RNA extracted from HD11 cells, cDNA was produced using SuperScript III reverse transcriptase, following the manufacture’s protocol (Thermo Scientific, Waltham, MA, USA). Samples were diluted in nuclease-free water in a 1:2.5 ratio. One μl of the diluted product was used for quantitative PCR (qPCR) in a final volume of 10 μl. qPCR was performed using SybrGreen Hi-Rox (PCR Biosystems Inc.) using primers described in Table 3
Fold change in mRNA expression was calculated by relative quantification using hypoxanthine phosphoribosyltransferase (HPRT) as endogenous control
Total RNA (up to 1 µg per reaction) from BMDM was reverse transcribed with iScript cDNA synthesis kit (Bio-Rad
Quantitative PCR was performed using 1 µl of cDNA
5 µl of iQ SYBR Green Supermix (Bio-Rad
0.25 µl of each primer pair and 3.5 µl of nuclease-free water in a total reaction volume of 10 µl
Fold-increase in gene expression was calculated by relative quantification using HPRT and Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as endogenous controls
HD11 WT cells were seeded at a confluence of 3x105 cells/ml in 12-well plates
The cells were primed with IFNα for 16 h and then with transfected exogenous DNA (HT- and CT-DNA – 2 μg/ml) or treated with 2’3’cGAMP (5 μg/ml) for 6 h
the cells were incubated with Zymosan coated beads conjugated with FITC at a ratio of 30 beads to 1 cell for all conditions for 40 min at 37°C
The cells were wash two times in PBS and fixed in suspension using the solution (missing ref; BD Biosciences) with 4% PFA
Cell populations were counted by analysis on a CytoFLEX cytometer
Fowlpox WT (FP9) and mutants [FPV012 (19) and FPV184 (20)] were propagated in primary chicken embryonic fibroblasts (CEFs) and grown in DMEM-F12 (Thermo Fisher Scientific
Ten-fold dilutions of cell supernatants were prepared in serum-free DMEM-F12 and used to inoculate confluent monolayers of CEFs for 1.5 h at 37°C
Cells were then overlaid with 2xMEM : CMC (1/1 ratio)
The foci were counted 7 days later after staining with Toluidine Blue
HD11 cells were seeded in 12-well plates in the day prior infection
Fowlpox viruses were diluted in serum-free DMEM-F12 at a multiplicity of infection (MOI) of 3 and added in the cells (1 ml per well)
Infected cells and supernatants were collected from infections at 8 and 24 h post-infection
Prism 7 (GraphPad) was used to generate graphs and perform statistical analysis
Data were analyzed using an unpaired t test with Welch’s correction unless stated otherwise
Data with P < 0.05 was considered significant and 2-tailed P-value were calculated and presented as: *p < 0.05
Each experiment has at least two biological replicates unless stated
indicating that this response is present in both primary macrophages and the transformed monocytic HD11 cell line
Figure 1 Intracellular DNA activates an IFN-I response in chicken macrophages
(A) HD11 cells were transfected with HT-DNA (1
CT-DNA (5 µg/ml) or Poly(I:C) and transcription of IFNB and ISG12.2 measured by qRT-PCR 6 h later
(B) Chicken BMDM were transfected with HT- DNA
CT-DNA (2 µg/ml) or Poly(I:C) (1 µg/ml) and transcription of IFNB and ISG12.2 measured by qRT-PCR 6 h later
(C) Resting BMDMs or BMDMs primed with IFNα for 6 h were transfected with HT- DNA
CT-DNA (2 µg/ml) or Poly(I:C) (1 µg/ml) and interferon activity in the supernatants was measured after 24 h using a bioassay
IFNα stimulation is a positive control in this assay
(D) HD11 or BMDM were primed with IFNα for 6 h
or Poly(I:C) and transcription of IFNB and ISG12.2 measured by qRT-PCR 6 h later
(E) HD11 (top) or IFNα-primed BMDM (bottom) were transfected with HT-DNA
or Poly(I:C) and cell viability measured by 7AAD staining 24 or 48 h later
***p < 0.001; ****p < 0.0001; ns: no significant difference
Data is representative of two or more replicates
cell death is likely not a specific output of STING signaling
key molecules involved in T cell activation by macrophages are regulated by DNA stimulation
but not all macrophage effector functions are equally enhanced by this signal
Figure 2 Intracellular DNA stimulates transcription of MHC-II and co-stimulatory molecules
(A) BMDMs or (B) HD11 cells were transfected with HT-DNA
and CD86 measured by qRT-PCR 6 h later
(C) HD11 cells were stimulated with HT-DNA
or Poly(I:C) and 6 h later phagocytosis was monitored by FITC-conjugated
Histograms of non-treated versus treated cells (left panels) and respective percentages of FITC positive cells for each treatment tested (right panel) are presented
Figure 3 STING and TBK1 contribute to DNA-driven transcriptional responses in chicken BMDMs
(A) HD11 and (B) BMDM cells were treated with 2’3’cGAMP (10 μg/ml) and qRT-PCR carried out 6 h later for the indicated genes
(C) BMDM were treated with the STING inhibitor H-151 (10 uM) or TBK1 inhibitor BX795 (1 uM) for 1 h before transfection with HT-DNA and CT-DNA
RNA was extracted and qRT-PCR carried out for the indicated genes
(D) BMDM were treated with the STING inhibitor H-151 (10 uM) or TBK1 inhibitor BX795 (1 uM) for 1 h before treatment with 2’3’cGAMP (10 μg/ml)
(E) HD11 cells were treated with 2’3’cGAMP (2.5 µg/ml) 6 h later phagocytosis was monitored by FITC-conjugated
These data confirm the intracellular DNA PRR function of cGAS in chicken macrophages
Figure 4 cGAS is essential for intracellular DNA-dependent IFN-I and MHC-II transcription in HD11 cells
(A) Example of identification of indel in clonally selected HD11 cGAS KO using NGS sequencing
(B) WT and cGAS KO HD11 cells were transfected with HT-DNA
CT-DNA (2 μg/ml) or Poly(I:C) (1 μg/ml) for 6 h and transcription of the indicated genes measured by qRT-PCR
(C) cGAS KO HD11 cells were primed with IFNα for 6 h
or Poly(I:C) and transcription of IFNB and ISG12.2 measured by qRT-PCR 6 h later (D) WT or cGAS KO cells were treated with 2’3’cGAMP (10 μg/ml) and transcription of IFNB measured by qRT-PCR 6 h later
In parallel, using the same methodology, we generated multiple STING knockout HD11 cell lines (Figure 5A). Stimulation of these cells with DNA phenocopied the cGAS knockout lines, and neither STING or cGAS KO altered tonic IFNB transcription, confirming the function of chicken STING downstream of cGAS in the intracellular DNA sensing pathway (Figure 5B, Supplementary Figures 4 and 5)
These data are consistent with the presence of a cGAS/STING pathway in HD11 cells and
in concert with the data using H151 in BMDMs
indicate the function of STING as a critical adaptor protein for intracellular DNA sensing in chicken macrophages
Figure 5 STING is essential for intracellular DNA-dependent IFN-I transcription in HD11 cells
(A) Example of identification of indel in clonally selected HD11 STING KO using NGS sequencing
(B) WT and STING KO HD11 cells were transfected with HT-DNA
CT-DNA (2 μg/ml) or Poly(I:C) (1 μg/ml) for 6 h and transcription of the indicated genes measured by qRT-PCR 6 h later
Figure 6 Fowlpox triggers a cGAS/STING dependent DNA sensing pathway in HD11 cells
(A) HD11 cells were infected with FWPV strain FP9 at a multiplicity of infection of three
cGAS or STING KO cells were infected with FP9 (black bars)
(D) HD11 cells were infected with FWPV strain FP9 at a multiplicity of infection of three
RNA was extracted and qRT-PCR carried out for the indicated FWPV genes
cGAS or STING KO cells were infected with FP9
or FPV184 at a multiplicity of infection of three
cell supernatants harvested and released FP9 was titrated on CEFs to measure focus forming units (ffu) per ml
The ability of innate immune cells to detect virus infection is dependent on a set of PRRs that directly bind viral nucleic acids. Macrophages act in this context as tissue-resident sentinel sensors of infection that express a broad repertoire of PRRs and mount a rapid and robust innate immune response to viruses and other pathogens. Indeed intracellular DNA sensing was first described in macrophages (25)
As well as interferon and cytokine production
activated macrophages use effector functions for pathogen clearance and for activation of adaptive immunity
In mammalian systems the signaling outputs downstream of intracellular DNA detection in macrophages include IRF-dependent IFN and cytokine production and cell death driven by the AIM2 inflammasome
we find that intracellular DNA sensing produces IFN but does not result in measurable cell death
rather it upregulates a specific set of antigen presentation machinery including the MHC-II gene BLB1 and co-stimulatory molecules
providing a direct link between anti-viral innate sensing and the initiation of adaptive immunity
Here we show that the cGAS/STING pathway in chicken macrophages can sense FWPV infection and is responsible for the IFN-I response as well as for upregulation of BLB1
but it remains to be seen how individual PRRs like cGAS contribute to protection against FWPV infection in vivo
In mice cGAS/STING are essential for the host response to poxvirus infections such as vaccinia and ectromelia viruses
and the protective effects are meditated via IFN-I
despite the presence of large numbers of immunomodulators targeting PRR signaling
including the cGAS/STING systems in these viruses
As such it is likely that cGAS/STING mediated FWPV DNA sensing and IFN-I production has a significant contribution to host defence against FWPV infection in chickens
although mechanistically it remains to be seen exactify how IFN-I mediates this defence against this avian poxvirus
Using CRISPR/Cas9 technology to knockout STING and cGAS in a transformed monocytic cell line (HD11) and complementing these data in primary macrophages with pharmacological inhibitors we have been able to show this cGAS/STING/TBK1 pathway is active in chicken macrophages
The use of primary cells in this context is important as transformation or immortalization can significantly alter PRR pathways so as to obscure physiological signaling mechanisms
Our data adds to the list of chicken cGAS/STING functions in sensing of avian DNA viruses such as MDV and Adenovirus 4 that replicate in the nucleus or FWPV that replicates in the cytoplasm
and in the regulation of macrophage effector functions
The ability of this pathway to sense a broad range of DNA viruses that replicate in different compartments in avian innate immune cells indicates that this pathway is a primary DNA sensing mechanism for DNA viruses in chickens
The raw data supporting the conclusions of this article will be made available by the authors
BF and CB provided the funding and supervised the work
and EK performed the experiments and statistical analysis
SG and MS generated the mutant fowlpox viruses
RG designed the study and wrote the manuscript
All authors contributed to the article and approved the submitted version
This work was funded by BBSRC grants BB/S001336/1 (BF and CB)
BB/H005323/1 & BB/K002465/1 (MS) and by EUROFERI (Région Centre-Val-de-Loire
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest
This manuscript has been released as a Pre-print at BioRxiv
We thank the experimental facility PFIE (Plateforme d’Infectiologie Expérimentale
France) for providing the animals used for the isolation of primary macrophages
The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fimmu.2020.613079/full#supplementary-material
Supplementary Figure1 | Effect of IFNα priming on expression levels of STING and IRF7 in BMDM and HD11
BMDM or HD11 cells were treated with IFNα for 6 h and transcription of STING and IRF7 measured by qRT-PCR 6 h later
Supplementary Figure 2 | BLB2 but not BLB1 is an ISG in HD11 cells
HD11 cells were treated with IFNα for 6 h and the indicated genes were measured by qRT-PCR
Supplementary Figure 3 | cGAS is essential for intracellular DNA-dependent IFN-I transcription in HD11 cells
WT or three individual cGAS knockout clones with different indels were stimulated with HT-DNA (2 μg/ml) and IFNB transcription measured by qRT-PCR 6 h later
Supplementary Figure 4 | STING is essential for intracellular DNA-dependent IFN-I transcription in HD11 cells
Supplementary Figure 5 | STING or cGAS loss does not significantly alter tonic IFN-I transcription
IFNB transcription measured by qRT-PCR in WT
cGAS KO or STING KO HD11 cells (data shown relative to WT cells)
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Received: 01 October 2020; Accepted: 16 December 2020;Published: 01 February 2021
Copyright © 2021 Oliveira, Rodrigues, Guillory, Kut, Giotis, Skinner, Guabiraba, Bryant and Ferguson. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY)
distribution or reproduction in other forums is permitted
provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited
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*Correspondence: Brian J. Ferguson, YmYyMzRAY2FtLmFjLnVr
†These authors share senior authorship
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Lipid mediators are known to play important roles in the onset and resolution phases of the inflammatory response in mammals
The phospholipid platelet-activating factor (PAF) is a pro-inflammatory lipid mediator which participates in vascular- and innate immunity-associated processes by increasing vascular permeability
by facilitating leukocyte adhesion to the endothelium
and by contributing to phagocyte activation
PAF exerts its function upon binding to its specific receptor
which is abundantly expressed in leukocytes and endothelial cells (ECs)
lipid mediators and their functions are still poorly characterized
and the role of PAF as an inflammatory mediator has not yet been investigated
In the present study we demonstrate that primary chicken macrophages express PAFR and lysophosphatidylcholine acyltransferase 2 (LPCAT2)
the latter being essential to PAF biosynthesis during inflammation
exogenous PAF treatment induces intracellular calcium increase
and increased phagocytosis by primary chicken macrophages in a PAFR-dependent manner
We also show that PAF contributes to the Escherichia coli lipopolysaccharide (LPS)-induced pro-inflammatory response and boosts the macrophage response to E
coli LPS via phosphatidylinositol 3-kinase/Akt- and calmodulin kinase II-mediated intracellular signaling pathways
Exogenous PAF treatment also increases avian pathogenic E
coli intracellular killing by chicken macrophages
and PAFR and LPCAT2 are upregulated in chicken lungs and liver during experimental pulmonary colibacillosis
exogenous PAF treatment increases cell permeability and upregulates the expression of genes coding for proteins involved in leukocyte adhesion to the endothelium in primary chicken endothelial cells (chAEC)
PAF boosts the chAEC inflammatory response to bacteria-associated molecular patterns in a PAFR-dependent manner
we identified PAF as an inflammation amplifier in chicken macrophages and ECs
which suggests that PAF could play important roles in the endothelium-innate immunity interface in birds during major bacterial infectious diseases such as colibacillosis
All these physiological or pathological processes have been well characterized in mammals
no study has addressed the putative regulatory roles for PAF in chickens during inflammation or infection
In line with that, PAF has been implicated in several animal models of lung injury, and treatment with PAF receptor antagonists attenuates endotoxin-induced lung injury (36). During pulmonary Gram-negative bacteria infection, PAF production is important for bacteria clearance (37). However, during experimental influenza A virus infection in mice, PAF plays a deleterious role by amplifying inflammation and tissue damage (38)
Despite a growing interest in characterizing early mediators of inflammation in chickens
and more notably their crosstalk with innate immunity sentinel cells such as macrophages
no previous works have addressed the mechanisms by which lipid mediators may contribute to inflammation or bacterial clearance
we aimed to characterize the PAF/PAFR interactions and to shed light on their functions in chicken macrophages and endothelial cells (ECs)
especially with respect to how PAF system molecules are modulated during pulmonary colibacillosis
Platelet-activating factor (synthetic PAF C16:0
β-acetyl-γ-O-hexadecyl-l-α-phosphatidylcholine hydrate
and 2′,7′-dichlorofluorescein diacetate (DCFDA
≥95% HPLC purity tested) were purchased from Sigma-Aldrich
>95% HPLC purity tested) and WEB 2086 (Apafant
PI3K/Akt inhibitor wortmannin (WMN; SL-2052
and calcium calmodulin kinase II (CaMK II) inhibitor KN62 (C38H35N5O6S2
>98% HPLC purity tested) were purchased from Tocris Biotechne
White leghorn chickens from the GB1 Athens inbred line (B13/B13 histocompatible chickens) or from the PA12 outbred line were hatched and raised specific-pathogen-free (SPF) at INRA (Plate-Forme d’Infectiologie Expérimentale
B13/B13 histocompatible chickens were housed in BSL2 poultry isolator units
HD11, an avian myelocytomatosis virus (MC29)-transformed chicken macrophage-like cell line (39)
UK) supplemented with 10% heat-inactivated fetal calf serum (FCS
and 100 µg/ml streptomycin (all from Sigma-Aldrich
UK) and grown routinely in a 75-cm2 flask (Corning
Chicken bone marrow-derived macrophages (BMDM) were outgrown from bone marrow cells using recombinant chicken macrophage colony-stimulating factor 1 (CSF-1) (40) derived from COS-7 cells (fibroblast-like cell line derived from monkey kidney tissue
USA) transfected with a pTArget vector (Promega
UK) expressing chicken CSF-1 (kindly provided by Prof
femurs and tibia of 3–4-week-old B13/B13 histocompatible or PA12 chickens were removed
and the marrow flushed with sterile phosphate-buffered saline (PBS
loaded onto an equal volume of Histopaque 1.077 gradient (Sigma-Aldrich
and centrifuged at 250 g for 30 min without brake
and cultured at a final concentration of 1 × 106 cells/ml in sterile 60 mm bacteriological plates (Corning
USA) in prewarmed complete RPMI-1640 medium supplemented with COS-7 supernatant containing chicken CSF-1
and 100 µg/ml streptomycin at 40°C under 5% CO2
Half of the medium was replaced with fresh
pre-warmed complete medium containing chicken CSF-1 at day 4
adherent cells were washed and harvested in cold PBS containing 2 mM ethylenediaminetetraacetic acid (EDTA
and resuspended in complete RPMI-1640 medium
All adherent cells presented macrophage-like morphology as evaluated in glass slides prepared in a CytoSpin® Cytocentrifuge (Shandon
97% of these cells were KUL01+ cells (a chicken macrophage marker) as evaluated by Flow Cytometry using a mouse anti-chicken monoclonal antibody (1:200 dilution
UK) and a rat-anti mouse phycoerythrin-coupled secondary antibody (1:300 dilution
Peripheral blood mononuclear cells (PBMC) were isolated from B13/B13 histocompatible chickens as previously described (41)
peripheral blood collected in EDTA-coated tubes was mixed with 1% methylcellulose (Sigma-Aldrich
1:1 v/v) and centrifuged at 25 g for 15 min
The upper phase was then diluted with PBS to the original volume of blood/methylcellulose mixture
carefully layered onto a Histopaque 1.077 gradient and centrifuged at 250 g for 30 min without brake
and resuspended in complete RPMI-1640 medium for further incubation at 40°C under 5% CO2
adherent cells presented monocyte/macrophage-like morphology as evaluated in glass slides prepared in a CytoSpin® Cytocentrifuge (Shandon
Primary chicken aortic endothelial cells (chAEC) were prepared from specific-pathogen-free (SPF) 18-day-old PA12 chicken embryos as previously described (42)
Primary chAEC were serially passaged (p2–p5) using 0.05% trypsin-EDTA (Gibco
UK) and kept in EC growth medium (EGM-2 BulletKit
Twelve-well tissue culture plates (Corning
USA) were seeded at 7 × 105 cells per well of HD-11 macrophage-like cells
or primary chAEC in complete medium and incubated at 40°C under 5% CO2 overnight prior to different stimulation protocols
LPS (10 ng/ml) and hPAF-AH (10 µg/ml) were previously diluted in RPMI-1640
and KN62 (1 µM) were previously diluted in DMSO
Dead bacteria [DB; APEC strain BEN2908 at 10 multiplicity of infection (MOI)
15 min incubation at 65°C for killing] were previously diluted in LB medium
Final concentration of DMSO (the vehicle used for the dilution of PAF
and cell signaling inhibitors) in cell culture wells never exceeded 0.1%
Treatment with PAF receptor antagonists or intracellular signaling pathway inhibitors was performed 1 h prior to stimulation
Cell culture supernatants were recovered 6 h after stimulation (unless otherwise indicated) and stocked at −20 or −80°C for subsequent analyses specified below
Cells were washed in sterile PBS and lysed with RNA lysis buffer (Macherey-Nagel
Germany) containing 2-mercaptoethanol (Merck Millipore
and stocked at −80°C until RNA extraction
For total protein quantification and Western blot (WB) analysis
cells were washed in PBS followed by cell lysis using RIPA buffer containing a cocktail of protease inhibitors
which also included phenylmethylsulfonyl fluoride and sodium orthovanadate (Santa Cruz Biotechnology
Primer pairs used in the present study for quantitative real-time PCR analysis
The Fluo-4 NW Calcium Assay kit (Molecular Probes
USA) was used to measure changes in HD11 cells’ intracellular calcium levels upon different stimuli
HD11 cells at 3 × 104 cells per well in a black 96-multiwell plate (Corning
USA) were loaded with 100 µl of the dye loading solution containing Fluo-4 NW dye and probenecid
according to the manufacturer’s instructions
The 96-well plate was incubated at 40°C under 5% CO2 for 30 min in the dark
and the stimuli of interest were added to the cells at T = 0
The changes in Fluo-4 NW fluorescence were measured at an excitation wavelength of 494 nm and an emission wavelength of 516 nm in a GloMax®-Multi Detection System plate reader (Promega
Calcium mobilization was recorded over time (213 s
To evaluate the pro-apoptotic and cytotoxic effects of different stimuli
cells were cultured as previously mentioned
Apoptotic/late apoptotic cells were identified using annexin V and propidium iodide (PI) double-positive staining strategy
and resuspended in an annexin-binding buffer (BD Biosciences)
annexin V-fluorescein isothiocyanate (FITC) was added to the cells for 30 min
the cells were further incubated with PI (BD Biosciences) for 15 min
stained cells (50,000 acquired events over total gated cells) were analyzed immediately using a BD FACSCalibur™ (BD Biosciences)
cell viability was determined using the colorimetric methylthiazoletetrazolium bromide (MTT) assay (Sigma-Aldrich
UK) that measures metabolic activity as a surrogate for cell viability/cytotoxicity
MTT was added to a final concentration of 5 μg/ml per well
and cells were incubated for 2 h at 40°C under 5% CO2
After complete solubilization of the dye using DMSO
plates were read at 550 nm in a Multiskan Ascent plate reader (Thermo Fisher Scientific
Caspase 3/7 activity was carried out using the Caspase-Glo 3/7 assay kit (Promega
UK) according to the manufacturer’s protocol
BMDM at 3 × 104 cells per well in a black 96-multiwell plate (Corning
USA) were incubated with different stimuli for 6 h
100 µl of Caspase-Glo 3/7 reagent was added to the wells
Plates were gently shaken and then incubated in the dark at 20°C for 60 min before luciferase activity was recorded using a GloMax®-Multi Detection System plate reader (Promega
The cell-penetrating dye 2′,7′-dichlorofluorescein diacetate (H2DCFDA) is oxidized by ROS to yield the fluorescent molecule 2′7′-dichlorofluorescein (DCFDA)
which is retained intracellularly and visible at the 488 nm excitation laser line
To evaluate ROS production upon different stimuli
BMDM were cultured as previously described and incubated with 10 µM H2DCFDA (Sigma-Aldrich
and cells receiving different stimuli were kept at 40°C under 5% CO2 for 2 h
Cells were then collected and washed in ice-cold PBS prior to flow cytometry analysis (50,000 acquired events over total gated cells) using a BD FACSCalibur™ (BD Biosciences
For the identification of PAFR expression in BMDM
and incubated for 2 h at 40°C under 5% CO2
washed in FACS buffer (2 mM EDTA and 2% FCS in PBS)
and stained with a rabbit polyclonal antibody raised against amino acids 1–300 of PAFR of human origin (Santa Cruz Biotechnology
and stained with a goat anti-rabbit IgG-FITC (Santa Cruz Biotechnology
and analyzed by flow cytometry (100,000 acquired events over total gated cells) using a BD FACSCalibur™ (BD Biosciences
Bone marrow-derived macrophages or HD11 cells were grown at 2 × 105 cells per well on sterile glass coverslips placed in 24-well plates containing complete medium and incubated at 40°C under 5% CO2 overnight
After adding the stimuli of interest for 2 h
cells were washed in PBS and fixed with 4% paraformaldehyde (Sigma-Aldrich
permeabilized with 0.5% Triton X-100 (Sigma-Aldrich
and 2% bovine serum albumin (Sigma-Aldrich
Immunostaining was performed with a rabbit polyclonal antibody raised against amino acids 1–300 of PAFR of human origin or rabbit polyclonal IgG as an isotype control (Santa Cruz Biotechnology
Secondary antibody goat anti-rabbit IgG-FITC (Santa Cruz Biotechnology
Cell nuclei were counterstained with ProLong Gold Antifade Mountant with DAPI (Thermo Fisher
Cells were observed under an Axiovert 200 M inverted epifluorescence microscope equipped with the Apotome imaging system (Zeiss
Images were captured with an Axiocam MRm camera and analyzed using the Axiovision software (Zeiss
Total protein from BMDM cell lysates was quantified using a Quick Start™ Bradford Protein Assay (Bio-Rad
Thirty micrograms of protein from whole cell lysates were mixed with 2× electrophoresis sample buffer (Santa Cruz Biotechnology
proteins were separated using 4–15% Mini-PROTEAN TGX™ Precast gels (Bio-Rad
USA) and transferred onto polyvinylidene difluoride (PVDF) membranes using a Trans-Blot® Turbo™ Mini PVDF Transfer pack (Bio-Rad
USA) in a Trans-Blot® Turbo™ Transfer system (Bio-Rad
The membranes were blocked in a buffer containing 5% non-fat dry milk in PBS for 1 h
Primary antibody targeting PAFR was the same as utilized for immunofluorescence (IF) staining at 1:500 dilution
a rabbit anti-Akt IgG polyclonal antibody (detecting endogenous levels of total Akt1
and Akt3 proteins—Cell Signaling Technology
a rabbit anti-CaMK II IgG polyclonal antibody (epitope corresponding to amino acids 1–300 mapping at the N-terminus of CaMK IIα of human origin
Mouse anti-glyceraldehyde-3-phosphate dehydrogenase IgG1 monoclonal antibody (GAPDH
Germany) was utilized as internal loading control at 1:1,000 dilution
primary antibodies diluted in 5% non-fat dry milk in PBS were added to the membranes for incubation overnight at 4°C under agitation
Following reaction with the primary antibodies
membranes were thoroughly washed in wash buffer containing 0.1% Tween 20 (Sigma-Aldrich
UK) in PBS and labeled with HRP-conjugated secondary antibodies (goat anti-rabbit or rabbit anti-mouse
the antigens were visualized using a Clarity™ ECL Western Blotting Substrate (Bio-Rad
USA) in a chemiluminescence FUSION FX apparatus (Vilber Lourmat
Bone marrow-derived macrophages were seeded at 2 × 105 cells per well in 24-well tissue culture plates
treated with different stimuli and immediately incubated with 10 µg/ml of Zymosan A (Saccharomyces cerevisiae) BioParticles™ Alexa Fluor™ 488 conjugate (Thermo Fisher Scientific
USA) in complete medium at 4°C or 40°C under 5% CO2 for 1 h
washed twice with ice-cold EDTA-containing PBS
Data were expressed as the percentage difference (delta) between fluorescence positive cells and cells incubated at 40°C (active phagocytosis) and 4°C (limited phagocytosis)
Nitrite (NaNO2) content was used as an index of nitric oxide (NO) production by chicken macrophages
Nitrite levels were determined in supernatants of BMDM
or HD11 cell cultures by spectrophotometry using the Griess reagent system (Promega
50 µl of the samples were added to 50 µl of freshly prepared Griess reagent in a 96-well plate
The absorbance was read at 550 nm in a Multiskan Ascent plate reader (Thermo Fisher Scientific
The nitrite concentration was calculated using a sodium nitrite standard curve
HD11 cells were seeded in 12-well plates at 5 × 105 cells per well and incubated at 40°C under 5% CO2 overnight. APEC strains BEN2908 [O2:K1:H5, a nalidixic acid-resistant derivative of strain MT78 which was isolated from the trachea of a chicken with respiratory infection (44)] and BEN3421 (O2:K1:H4
a nalidixic acid- and tetracyclin-resistant strain isolated from a chicken presenting colibacillosis in 2009 in France) were utilized for infection
Cell monolayers were infected with mid-log-phase bacteria at an MOI of 10 and incubated for 1 h in cell culture medium without FCS
Cells were washed and remaining extracellular bacteria were killed by incubation in complete medium containing gentamicin (100 µg/ml) for 1 h 30 min
A group of cells were then washed and lysed with sterile water for 30 min at 4°C to evaluate the percentage of invasion through bacterial enumeration by viable counts on LB agar plates
Percentage of invasion (T = 0) was calculated as the number of intracellular bacteria divided by the number of bacteria in the inoculum
and gentamicin concentration was reduced to 10 µg/ml (a concentration known to kill BEN2908 and BEN3421) to avoid putative accumulation within cells during prolonged incubation
PAF (1 or 10 µM) was added together with gentamicin
supernatant was recovered for nitrite dosage and stocked at −20°C
Cells were washed and lysed with RNA lysis buffer or sterile water for 30 min at 4°C
Intracellular bacteria were enumerated by viable counts on LB agar plates
Percentage of growth was calculated as the number of intracellular bacteria at a given time point divided by the number of bacteria at T = 0
Four-week-old B13/B13 histocompatible chickens were infected intratracheally with 109 colony-forming units of the highly adhesive/invasive APEC strain BEN2908 in 200 µl of sterile endotoxin-free NaCl 0.9% solution
The inoculum was prepared with bacteria in the mid-log-phase of growth
The control group was inoculated with sterile NaCl 0.9% solution
Lung and liver samples were collected aseptically from each chicken 6 h post bacterial inoculation
Tissue samples for RNA extraction were snap frozen in liquid nitrogen and stocked at −80°C
placed in gentleMACS™ C tubes containing sterile PBS
and homogenized using a gentle MACS™ Dissociator (Miltenyi Biotec
Dilutions of lung homogenates were plated onto Drigalski agar plates supplemented with nalidixic acid (30 µg/ml) for bacterial quantification
and 1 ml was incubated in brain heart infusion for qualitative detection of E
Primary chAEC were seeded at a density of 5 × 104 cells on fibronectin-coated Falcon® Permeable Support (8.0 µm pore) PET membranes (Corning
placed in 24-well plates containing EC medium and cultured for 72 h at 40°C under 5% CO2
chAEC monolayers in the upper chamber received different stimuli and
EC growth medium containing 1 mg/ml FITC-dextran (40,000 MW) (Sigma-Aldrich
UK) was added followed by further incubation for 30 min at 40°C under 5% CO2
50 µl were collected from the lower chamber
and fluorescence signals relating to FITC-dextran passage from the upper to the lower chamber were measured using a GloMax®-Multi Detection System plate reader (Promega
Cell layer permeability was expressed as fold increase in FITC-dextran fluorescence as compared to the control group (vehicle)
and Gallus gallus: XP_004947758) and LPCAT2 (H
Comparisons between two groups were performed using a two-tailed unpaired Student’s t test
Multiple groups were compared using a one-way analysis of variance followed by a Newman–Keuls multiple comparison post hoc test
Values for all measurements are expressed as mean ± SEM
P < 0.05 was considered statistically significant
Statistical analyses were performed using GraphPad Prism 5.0 (GraphPad Software
Data are representative of at least two independent experiments
Chicken PAFR also contains two conserved predicted sites for N-linked glycosylation and nine threonine (T) or serine (S) residues identified as potential sites for phosphorylation by protein kinase A
or C (Figure S1 in Supplementary Material)
Components of the platelet-activating factor (PAF) system are expressed in chickens
and exogenous PAF induces intracellular calcium increase in chicken macrophages
(A) The gene expressions of PAF receptor (PAFR)/PTAFR and (B) LPCAT2/LPCAT2 were evaluated by quantitative real-time PCR (qRT-PCR) in unstimulated chicken tissues and macrophages [HD11 macrophage-like cells
bone marrow-derived macrophages (BMDM) and peripheral blood mononuclear cells (PBMC)]
(C) PAFR/PTAFR gene expression was evaluated by qRT-PCR in purified bone marrow cells following chCSF-1 medium complementation for BMDM differentiation from days 0 to 7
Data are expressed as relative normalized expression (as compared to two housekeeping genes)
In (D,E) the HD11 cell line was stimulated with PAF and/or PAFR antagonists (PCA 4248 and WEB 2086)
and the increase in intracellular calcium signal was recorded over time (216 s
This suggests that PAF seems to act in a specific receptor (PAFR)-mediated fashion in chicken macrophages as in mammalian cells
these data revealed that PAFR is expressed at the protein level and can be downregulated and partially degraded by PAF in chicken macrophages
Platelet-activating factor receptor (PAFR) protein expression in chicken primary macrophages can be modulated by exogenous platelet-activating factor (PAF) or lipopolysaccharide (LPS)
(A) Immunofluorescence (IF) analysis of PAFR protein expression using an anti-PAFR polyclonal antibody
in B13/B13 histocompatible chicken bone marrow-derived macrophages (BMDM)
BMDM were stimulated with PAF (10 µM)
Escherichia coli LPS (10 ng/ml) or PCA 4248 (10 µM) for 2 h before IF analysis
PAFR expression is shown in green (Alexa-Fluor 488-conjugated secondary antibody) and the nucleus in blue (DAPI staining)
(B) Representative flow cytometry dot plots showing gating strategy for PAFR expression analysis in BMDM and histogram showing PAFR expression upon BMDM stimulation for 2 h with PAF and/or PCA 4248 as compared to isotype control
(C) Western blot analysis of PAFR expression in BMDM whole cell lysates following different treatments for 2 h
Target protein size is indicated with black arrows
(D) PAFR/PTAFR and LPCAT2/LPCAT2 gene expression analysis in BMDM stimulated with PAF
or dead bacteria (10 multiplicity of infection) for 6 h
Data are expressed as relative normalized expression (as compared to vehicle control group)
IF images were captured using an Axiovert 200 M inverted epi-fluorescence microscope equipped with an EC Plan-Neofluar 40 × /1.3 oil/Dic objective (ApoTome system
**P < 0.01 when compared to negative (vehicle) control group
#P < 0.05 when compared to positive control groups
In addition to this physiological phenomenon, we observed that PAFR gene expression is increased upon E. coli LPS or DB stimulation, but not upon exogenous PAF treatment, for 6 h as compared to vehicle-treated group (Figure 2D), as was assessed by IF analysis (Figure 2A
LPCAT2 gene expression was also upregulated by these pro-inflammatory bacterial stimuli
which suggests that bacteria-associated molecular patterns are positive signals for the upregulation of PAFR and LPCAT2 genes
the latter being important for the metabolism of PAF during inflammation
To further address the functional role of PAF in chicken primary macrophages, we first assessed whether exogenous PAF were cytotoxic to these cells. We showed that PAF (1 and 10 µM) was not cytotoxic to chicken BMDM after 6 h stimulation as evaluated through annexin V/PI double-staining strategy (Figure 3A) and caspase 3–7 activation assay (Figure 3B)
both canonical markers for early and late cell apoptosis
coli LPS and DB were cytotoxic to chicken BMDM within the same experimental settings
Exogenous platelet-activating factor (PAF) treatment does not impact cell viability and induces reactive oxygen species (ROS) release by chicken primary macrophages
(A) Representative flow cytometry dot plot and bar graph showing gating strategy for annexin V and propidium iodide (PI) expression analysis in bone marrow-derived macrophages (BMDM) from B13/B13 histocompatible chicken and percentage of double-positive stained cells
following treatment with PCA 4248 (10 µM)
Escherichia coli lipopolysaccharide (LPS) (10 ng/ml) or dead bacteria (10 multiplicity of infection) for 6 h
(B) Caspase 3–7 activity in BMDM following exposure to different stimuli for 6 h
(C) Delta percentage of BMDM containing zymosan-fluorescein isothiocyanate particles following different stimuli for 1 h as an index of phagocytosis (delta calculated after incubation at 4°C and 40°C)
(D) Representative flow cytometry dot plot and histograms showing ROS release by BMDM
as determined by intracellular DCFDA fluorescence intensity
(E) Bar graph showing the mean fluorescence intensity (MFI) of DCFDA-positive BMDM following different stimuli for 2 h
**P < 0.01 when compared to negative (vehicle or medium) control groups
We next asked whether PAF could enhance BMDM phagocytosis of fluorescent zymosan beads. We observed that PAF (10 µM) treatment for 1 h significantly enhanced chicken macrophage phagocytosis and that PAFR antagonist PCA 4248 abrogated this phenomenon (Figure 3C)
In another biologically relevant assay, we assessed whether PAF induces ROS release by chicken macrophages. Using a fluorescent probe, we showed that both PAF (10 µM) and E. coli LPS stimulation for 2 h promoted enhanced ROS release by chicken BMDM. However, PAFR antagonist PCA 4248 reverted ROS release only in PAF-treated BMDM, revealing that ROS release is induced by PAF in a PAFR-dependent manner (Figures 3D,E)
Altogether these data suggest that PAF promotes two acute macrophage-related inflammatory events in a PAFR-dependent fashion and independent of any cytotoxic effect in chicken macrophages
These data suggest that PAF produced by chicken macrophages upon LPS stimulation contributes to the overall pro-inflammatory effects of LPS via PAFR
Endogenous platelet-activating factor (PAF) contributes to the pro-inflammatory response elicited by lipopolysaccharide (LPS) and exogenous PAF potentiates LPS-induced inflammation in chicken primary macrophages
coli LPS (10 ng/ml) in the presence or absence of PCA 4248 (10 µM) or human PAF-acetylhydrolase (PAF-AH) (10 µg/ml) for 6 h
B13/B13 histocompatible chicken-derived bone marrow-derived macrophage (BMDM) supernatants were assessed for the presence of (A) nitric oxide (NO)
and cell lysates were used to analyze gene expression of (B) iNOS/NOS2
and (D) IL-1β/IL1B by quantitative real-time PCR
(E) PAF (0.1–10 µM) alone or together with LPS was added to BMDM
and NO production in the supernatants was assessed after 6 h
(F) NO production by BMDM derived from the bone marrow of the outbred PA12 chickens following exposure to PAF (10 µM) and/or LPS in the presence or absence of PCA 4248 (10 µM) for 6 h
(G) NO production by peripheral blood mononuclear cells (PBMC) from B13/B13 histocompatible chickens following exposure to PAF (10 µM) and/or LPS in the presence or absence of PCA 4248 (10 µM) for 6 h
and ***P < 0.001 when compared to negative (vehicle) control groups
#P < 0.05 and ##P < 0.01 when compared to positive control groups
Exogenous platelet-activating factor (PAF) potentiates the pro-inflammatory response elicited by lipopolysaccharide (LPS) in chicken primary macrophages in a PAF receptor (PAFR)-dependent manner
After 6 h stimulation with PAF (10 µM) and/or E
coli LPS (10 ng/ml) in the presence or absence of PAFR antagonist PCA 4248 (10 µM)
B13/B13 histocompatible chicken-derived bone marrow-derived macrophage (BMDM) supernatants were assessed for the presence of (A) nitric oxide
and (D) COX-2/PTGS2 by quantitative real-time PCR
(E) Prostaglandin E2 dosage by mass spectrometry in BMDM supernatants following the same aforementioned stimuli for 6 h
**P < 0.01 and ***P < 0.001 when compared to negative (vehicle) control groups
in a magnitude that does not appear to interfere with their inhibitory action on PAFR signaling and its potentiation effects as suggested
We did not observe any statistically significant effects in the aforementioned parameters when the p38 MAPK-mediated signaling pathway was blocked using the specific inhibitor SB 203580 (data not shown)
The potentiation effects of platelet-activating factor (PAF) on lipopolysaccharide (LPS)-induced pro-inflammatory response in chicken primary macrophages are partially dependent on CaM KII- and phosphatidylinositol 3-kinase (PI3K)/Akt-mediated signaling pathways
After 6 h stimulation with PAF (10 µM) and/or Escherichia coli LPS (10 ng/ml) in the presence or absence of PI3K antagonist wortmannin (WMN
(E) Delta percentage of BMDM containing zymosan-fluorescein isothiocyanate particles following different stimuli for 1 h as an index of phagocytosis (delta calculated after incubation at 4°C and 40°C)
(F) Western blot analysis of CaM KII and Akt expression in BMDM whole cell lysates following different treatments for 6 h
**P < 0.01 and ***P < 0.001 when compared to negative (vehicle or medium) control groups
We also confirmed that Akt (which is phosphorylated by PI3K) and CaMK II are expressed in chicken BMDM at protein levels (Figure 6F)
although we could not determine the presence of PI3K due to the unavailability of validated commercial antibodies known to recognize this enzyme in chickens
We therefore presume that PAF exerts its pro-phagocytic and potentiating effects over LPS-induced pro-inflammatory responses through PI3K/Akt- and/or CaMK II-mediated intracellular signaling pathways
we showed that PAF is able to promote increased intracellular bacteria killing together with an increased pro-inflammatory response
we suggest that APEC infection is likely to promote increased PAF signaling and production by chicken macrophages
Exogenous platelet-activating factor (PAF) treatment favors intracellular bacteria killing and amplifies the inflammatory response in infected chicken macrophages
(A) HD11 macrophage-like cells were infected with 10 multiplicity of infection (MOI) of avian pathogenic Escherichia coli (APEC) strains BEN2908 or BEN3421 (both O2 serotype strains) followed by treatment with PAF (1 or 10 µM) for 6 or 24 h
Intracellular bacterial load was evaluated through colony-forming unit counts
(B) Cell viability was evaluated through a colorimetric assay based on methylthiazoletetrazolium bromide cellular metabolism
following the same in vitro infection protocol
Data are expressed in optical density at 550 nm
(C) Nitric oxide production in the supernatants of HD11 cells following infection with 10 MOI of APEC BEN2908 in the presence or absence of PAF
(D) Immunofluorescence (IF) analysis of PAF receptor (PAFR) protein expression using an anti-PAFR polyclonal antibody
PAFR expression is shown in green (Alexa-Fluor 488-conjugated secondary antibody) and the nucleus in blue (DAPI immunostaining)
(E) PAFR/PTAFR and (F) LPCAT2/LPCAT2 gene expression analysis in HD11 cells following infection with 10 MOI of the APEC BEN2908 strain
Quantitative real-time PCR data are expressed as relative normalized expression (as compared to vehicle control group)
and ***P < 0.001 when compared to negative (vehicle or medium) control groups
the gene expressions of PAFR/PTAFR and LPCAT2/LPCAT2 are upregulated together with pro-inflammatory gene expression such as COX-2/PTGS2
and IL-1β/IL1B as compared to vehicle-instilled animals
These data suggest that during pulmonary colibacillosis
and metabolism are overexpressed concomitantly to genes related to the acute inflammatory response
which is in agreement with the data found in APEC-infected macrophages
Overexpression of platelet-activating factor receptor (PAFR) and LPCAT2 is correlated with increased pro-inflammatory gene expression in chicken organs during pulmonary colibacillosis
(A) Bacterial load in the lungs of B13/B13 histocompatible white leghorn chickens at 6 h following intratracheal infection with 109 colony forming units of APEC BEN2908 (O2 serotype) strain
(B) Lung or (C) liver samples from APEC BEN2908-infected chickens were analyzed for PAFR/PTAFR
and IL-1β/IL1B gene expression by quantitative real-time PCR
***P < 0.001 when compared to negative (vehicle) control group
these data reveal that PAF is active in chicken endothelial cells and promotes increased cell permeability
potentiates bacterial-derived inflammatory responses
and may indirectly contribute to leukocyte adhesion to the chicken endothelium
Exogenous platelet-activating factor (PAF) contributes to chicken endothelial cell dysfunction and increased pro-inflammatory response to bacteria-associated molecular patterns
(A) PAF receptor (PAFR)/PTAFR gene expression
as evaluated by quantitative real-time PCR (qRT-PCR) analysis
in chicken aortic endothelial cells (chAEC) from PA12 outbred chickens following treatment with PAF (10 µM)
(B) Fluorescein isothiocyanate (FITC)-dextran relative fluorescence units (RFU)
as an index of chAEC monolayer permeability in a transwell system
following treatment with PAF (1 or 10 µM) in the presence or absence of PCA 4248 (10 µM)
(C) FITC-dextran RFU in the same transwell system at 30 min post chAEC treatment with PAF in the presence or absence of PCA 4248
Data are expressed as fold increase as compared to vehicle control group
as evaluated through a colorimetric assay based on methylthiazoletetrazolium bromide cellular metabolism
(E) IL-1β/IL1B and (F) CXCLi2/IL8L2 gene expression in chAEC following treatment with PAF
and DB for 6 h in the presence or absence of PCA 4248
qRT-PCR data are expressed as relative normalized expression (as compared to vehicle control group)
and ###P < 0.001 when compared to positive control groups
Exogenous platelet-activating factor receptor (PAF) directly promotes upregulation of adhesion molecules gene expression in chicken endothelial cells
(A) E-selectin/SELE and (B) VCAM-1/VCAM1 gene expression in chicken aortic endothelial cells (chAEC) following treatment with PAF (10 µM)
*P < 0.05 and **P < 0.01 when compared to negative (vehicle) control groups
The physiological and pathological roles of lipid mediators in livestock animals
are often neglected and little is known on their presence and mechanisms of action
we provide novel insights into the function of PAF as a pro-inflammatory mediator in chickens and the mechanism through which PAF contributes to chicken macrophage activation and responses to bacterial LPS
PAF contributes to intracellular bacterial killing and EC dysfunction
two phenomena that may be correlated with the overexpression of PAFR and LPCAT2 in organs of chickens presenting colibacillosis
we provided evidence that PAF may be an early orchestrator of the inflammatory response to pathogenic bacteria in chickens
paracrine- or autocrine-produced PAF is likely to play a direct role in the inflammatory response to Gram-negative bacteria-associated molecular patterns in chickens
notably at the toll-like receptor 4 (TLR4) level
The biological relevance of these findings merits to be further investigated in vivo
as suggested by the data in the present manuscript
the contribution of PAF to heterophil (the avian ortholog of neutrophils) arrest and recruitment via PI3K/Akt signaling pathway merits to be investigated
this is the first study highlighting the role of a lipid mediator in promoting EC dysfunction in chickens
PAF treatment led to the upregulation of genes coding for the leukocyte adhesion molecules VCAM-1 and E-selectin
produced within the endothelium and adjacent tissues
could favor not only leukocyte activation but also leukocyte arrest and recruitment
and ECs during host-response to Gram-negative bacteria could contribute to local and sustained inflammatory responses in chickens
we demonstrated that PAF is able to promote increased bacterial clearance by primary chicken macrophages in vitro
together with a strong amplification of the inflammatory response
Our gene expression data showed that PAFR and LPCAT2 genes are overexpressed in lungs and liver of APEC-infected chickens at early time points postinfection
While these data reveal that key components of PAF recognition and biosynthesis are locally expressed in parallel to a strong inflammatory response to APEC
we are still unable to define which cell populations are expressing these molecules
it is reasonable to assume that PAF is indeed produced and acts within infected sites
thereby amplifying inflammation and/or contributing to bacterial clearance as observed in vitro
Both PAFR and LPCAT2 genes are overexpressed in chicken macrophages and chAEC upon LPS stimulation in vitro
which suggests that at least these cell types may be involved in the response to colibacillosis in vivo
LPCAT2 is believed to be the main pro-inflammatory LPCAT in the remodeling pathway for the biosynthesis of PAF in mammals
Our protein homology data suggest that chicken LPCAT2 is closely related to human and mouse counterparts
upon contact with bacteria or bacteria-associated molecular patterns
and other unidentified tissue parenchyma cells
PAF would in turn amplify local inflammation through eicosanoid
and chemokine production to facilitate initial bacterial clearance and trigger the inflammatory response
parenchymal) and endothelial PAF production would directly or indirectly (e.g.
via chemokine production) promote increased leukocyte adhesion and recruitment (e.g.
contributing to the orchestration of classical cellular and molecular events that take place at the onset of the inflammatory response
We therefore suggest that PAF might be an important mediator of inflammation in the host response to Gram-negative bacteria causing economically relevant diseases in poultry farms worldwide
and a proof of concept on the use of PAFR antagonists to limit exacerbated inflammation associated with experimental colibacillosis are currently being performed
Although the feasibility of such therapeutic strategy in the poultry industry is still difficult to envisage
these experiments will bring biologically relevant information on how lipid mediators and their receptors could be pharmacologically manipulated in chickens
so as to pave the way to alternative therapies in face of the widespread antibiotic resistance in poultry farms and the lack of efficacious vaccines for certain avian diseases
we believe that the present study sheds light on the role and function of PAF in bridging endothelium function and macrophage-associated innate immunity in chickens in response to bacteria-derived stimuli
these activity profiles may be shared by other yet to be identified lipid mediators of inflammation
a line of research that should be of interest to the scientific community in the fields of avian immunology
All animals used in the avian pathogenic Escherichia coli (APEC) infection protocol were treated according to EU recommendations for animal welfare
and the protocol was approved by the French regional ethics committee number 19 (Comité d’Ethique en Expérimentation Animale Val de Loire) under the reference CL2007-44
and AL performed the experiments and analyzed data
The reviewer TK and handling editor declared their shared affiliation
We thank Nathalie Lallier for her technical assistance on the experimental infection model and the personnel from the experimental unit PFIE (Plateforme d’Infectiologie Expérimentale) at the Centre INRA Val de Loire (Nouzilly
Brazil) for valuable discussions on the experimental design setup
This work was supported by the French National Institute for Agricultural Research (INRA) through a young researcher grant (to RG) from the Animal Health division (Département Santé Animale
The Supplementary Material for this article can be found online at http://www.frontiersin.org/articles/10.3389/fvets.2017.00226/full#supplementary-material
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Keywords: avian pathogenic Escherichia coli
Schouler C and Guabiraba R (2017) Characterization of the Phospholipid Platelet-Activating Factor As a Mediator of Inflammation in Chickens
Received: 19 October 2017; Accepted: 06 December 2017; Published: 18 December 2017
Copyright: © 2017 Garrido, Chanteloup, Trotereau, Lion, Bailleul, Esnault, Trapp, Quéré, Schouler and Guabiraba. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY)
provided the original author(s) or licensor are credited and that the original publication in this journal is cited
*Correspondence: Rodrigo Guabiraba, cm9kcmlnby5ndWFiaXJhYmEtYnJpdG9AaW5yYS5mcg==
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we have chosen five municipalities as pilot municipalities of the Healthy Municipalities Project
They are located in "Central Agreste" region (the Agreste region lies between the coastal rainforest region and instate semiarid lands of Northeast
We took into consideration the economic situation
the existence or lack of similar projects and the willingness of the municipality to collaborate
These 5 municipalities are between 110 to 130km from the state capital of Recife
All have agriculture and livestock farming as the major industry
The total population of these 5 municipalities is 97,295 (in the year 2000) and their Human Development Index is 0.588 (in 2000)
Their HDI is practically at the level considered for low-income countries (0.554 in the 2000 Human Development Report)
which has previously have worked with Healthy Municipalities aided by the Ministry of Health
is also integrated as one of the pilot municipalities of the project
We then selected pilot communities in each municipality
we chose one life cycle as a theme for each municipality through interviews and existing information
we selected one community from each pilot municipality - the community with an accumulation of social capital relevant to the selected life cycle
we selected the youth life cycle theme in Bonito
We selected one pilot community where there were a large number of youth groups
Figure5 : Localization of Pilot Municipalities
In the concept of Healthy Municipalities, health would be improved not only through improvements to health care services, but also by the effects of various factors in everyday life (q.v. Figure 2)
We call this the "Idea of Comprehensive Health"
we should not treat health and life within only a few sectors such as health care
education or industries; we should treat them more widely and cross-sectionally
the framework of the life cycle comes to the fore
Thinking in terms of life cycle phases such as children
we can treat health and life in a more comprehensive fashion
Our Healthy Municipalities Project proposes the life cycle framework and performs trial runs of specific policy-making and intersectoral cooperation
This is just a gateway of activities and it is possible for each pilot municipality to alter or amplify the life cycle themes later on
The life cycle themes of each municipality are cited below
Barra de Guabiraba The life cycle theme : adult men
Camocim de São Felix The life cycle theme : adult women and children
Sairé The life cycle theme : elderly
São Joaquim do Monte The life cycle theme : adult women and children
Itambé The life cycle theme : infants
municipality and community development takes a long time
All precedent cases of municipality and community building generally show that there are no concrete outcomes at first
but they become gradually clear in the process of 3 to 5 years
Particularly when involving the development of human resources and social capital (capacity development)
it is important to support development with patience as well as considerable time and effort
in supporting "municipality and community development" through a technical cooperation project that calls for certain results within limited time
the Healthy Municipalities Project has chosen as its objective the creation and implementation of "mechanisms" that may be developed and concretized during the project period
"Mechanisms" are social devices that permit continuity in the collaborated activities of residents and local government
There are three different levels on which where these activities are implemented
Figure6 : Mechanism of Healthy Municipalities
residents freely discuss and take an active part in the undertakings
Facilitators have the role of encouraging community gatherings and leading meetings
"Facilitators" work in cooperation with "supervisors" (mentioned later) to promote community activities
always seeking to have new members participate in them
The participation of "collaborators of healthy municipalities" who help facilitators and supervisors is also indispensable
there is EAPPPS (Center for Healthy Public Policy Articulation and Promotion) for the integration and coordination of public policies giving priority to health and life
Supervisors coordinate and link activities from the micro and mid levels here
these include the intersectoral adjustment of public policies that reflect the concerns of the residents
the training of the human resources necessary for Healthy Municipalities
implementation and evaluation of community activities
the coordination of federal and state government programs or projects to meet the community's needs
participation in the development planning of municipalities
On the macro level (group of adjacent municipalities)
there arise discussions on broad-based common issues that can be more effectively resolved together than by an individual municipality
as the referral center for "Healthy Municipalities"
the UFPE trains the necessary human resources for the "mechanisms" and lend technical support to the activities
The UFPE also hosts the network of healthy municipalities and diffuses the "mechanisms" to other regions
the state government has introduced "Healthy Municipalities" in its development strategy and offers information on various public programs or projects to the EAPPPS of each municipality to support the planning of healthy public policies
In the course of the discussions on the intervention method of the Healthy Municipalities Project in communities
the central issue was how a community becomes empowered (how is it possible to improve the autonomy of the community effectively)
There are two fundamental problems in this region
people who live in Northeast region of Brazil have historically leaned heavily upon the hope of assistance from patrons
the notion of autonomy within the community is fragile
it is desirable for the community to solve their problems themselves through the empowerment process
but there is difficulty in achieving this with community efforts alone due to the serious problems stemming from poverty
Dealing with these two problems simultaneously is daunting
we need to take a different path from conventional ways
we have developed a method that seeks to make the best use of Existing Potentials (utilizing the abilities of one person who is good at making things
etc.) in the community to set up goals that can be accomplished by the community itself
We believe that their autonomy can be enhanced by achieving these goals
(The traditional approach has been a "cause-seeking approach" that analyzes the cause of problems to be solved.) The development of project method is based on the SOJO (System-Oriented Joyful Operation) model developed by Japanese researcher Toshihiro IWANAGA and others
people feel a sense of accomplishment through the implementation of small actions through joint efforts
boosting their self-respect and lending continuity for further actions with confidence
This name derives from the image of bamboo: Flexibility - flexible application of the method is one aspect; the firm roots of bamboo - a sound base in reality and also symbolizes the collaboration of Brazil with the Orient
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Volume 7 - 2016 | https://doi.org/10.3389/fimmu.2016.00125
Immunology developed under the notion of the immune system exists to fight pathogens
the discovery of interactions with commensal microbiota that are essential to human health initiated a change in this old paradigm
we argue that the immune system has major physiological roles extending far beyond defending the host
Immune and inflammatory responses share the core property of sensing
defining the immune system also as a sensory system
The inference with the immune system collects
places it in close relationship to the nervous system
which suggests that these systems may have a profound evolutionary connection
indicating its theoretical basis should be updated
There is a consensus among scientists that the ability of microorganisms or microbial products to trigger inflammation and immune responses are important for immune function
We would like to suggest that immune functions extend far beyond interaction with pathogens
targeting the host immune response instead of the causative agent itself may be an effective option in the context of disease
inflammation is prone to imbalance as many physiological machineries in the organism
and loss of balance relates to pathogenic states
we argue that inflammation and innate immunity are biological-related processes
which must operate under similar premises and toward the common goal of reaching homeostasis
Figure 1. Incorporation of inflammation into immunology. Over the last decades, inflammation and immunology were progressively merged as biomedical research evolves. (A) Scientific papers, in numbers, retrieved from queries for “immunology,” “inflammation AND immunology,” and “inflammation” at PubMed (http://www.ncbi.nlm.nih.gov/pubmed)
Results span 1 year (forth to fifth year) over four consecutive decades (80’ to 2010’)
(B) Scientific papers retrieved from “immunology” for the given year/decade were queried for “inflammation,” and vice versa
Exposure to microbiota or to microbial products promptly restores the ability of germ-free mice to respond as conventional mice
indicating that the immune tissues and cells were present and functional in the absence of microbes
This concept of responsiveness to host leads to broader considerations
that the immune system does not depend on pathogens to function or exist
Biomedical research is biased toward disease
although disease does not represent homeostasis in the vertebrate host
thus the immune system must operate in such spectrum
The pyramid estimates the proportion of immune responses that go unnoticed by current experimental techniques in cold colors
in comparison to less frequent immune responses in the context of disease
immune responses are categorized by abundance and intensity
the categories of inflammation are depicted
If the immune system is part of a living functioning organism, constantly reaching for homeostasis, interacting with microbiota, remodeling tissue, dealing with injury, and so forth; interacting with pathogens is a small fraction of the activities of the immune system (27). Contact with a pathogen may result in infection, and infection could lead to disease (28)
Based on these possibilities and the fact that the immune system is fully active for a lifetime
given the impact of disease in human health
it comes as no surprise that biomedical research is focused on disease
though disease does not represent or explain homeostasis between systems in a host
Although extensive knowledge on disease allows us to explore it and propose treatments
the challenge relies on studying processes that did not lead to disease
The greatest challenge in reinterpreting the immune system is to define what the system is and what it does to maintain homeostasis. The basis for that may be the overlap of inflammation and immune responses. In terms of core mechanism, their common ground is sensing and recognition of molecules of variable compositions, forms, sources, and properties (14)
the immune system is unable to respond or to sustain interaction
inflammation is unable to start or to resolve
the ability of the immune system to sense things is not conflicting with sustaining interactions with both microbes and host
we propose that the immune system is a sensory system
vascular tissues are in constant scrutiny by circulating leukocytes
These interpretations can be exemplified by the combination of signals (cytokines
and antibodies) that define leukocyte recruitment
which stands for information interpretation and reply
the bulk of information that the immune system manages is what allows the system to define and pursue homeostasis
Information management by the immune system
The nervous and immune systems handle large volumes of information
the immune system contributes to host homeostasis
This process start with information sensing
obtained through interaction with molecules of different origins and composition
causing specific leukocyte activation and recruitment
information is communicated and replied to other components of the immune system
such as in antigen-presenting cells and T CD4+ lymphocytes
The immune system is able to store information
for which adaptive memory is the most studied process
Stored information can be promptly accessed
exemplified by quick adaptive immune responses upon secondary challenges
adding to the ongoing flow of information through the immune system
those examples corroborate our hypothesis by showing how specialized the immune system is to sense and manage alterations in the host homeostasis (e.g.
over other body systems not directly involved in sensing
in case of intrinsic failure of the immune system
a simple stimulus could lead to disastrous consequences
Inferring that the immune system plays an important role in sustaining intrahost interactions would also explain why immune responses and inflammation have great influence over other host systems
immunity can be described as a host system of information management
which allows all possible interactions the host may have to sustain
The nervous system is traditionally associated with sensing and management of information in the vertebrate host
The suggestion that the primary function of the immune system is also sensing and management of information may be conflicting
since these are already entrusted to another evolutionary-conserved body system
sensing is a general property of multicellular organisms and essential for host fitness
Although it may appear controversial to have two complex systems in charge of the same function
the nervous and immune systems are not redundant
These systems mediate interactions between host and environment that exceed interactions made by any other body systems in number and complexity
The nervous and immune systems share remarkable similarities
such as full coverage of the host and interactivity
The nervous system is responsible for sensing physical stimuli
This panel is complemented by the immune system’s sensing of chemical stimuli
both systems confer a notion of “self” to the host
by defining what the host is from different perspectives
The notion of self is a key aspect for interaction between the host and other organisms
these systems could manage immeasurable amounts of information and interaction in vertebrate organisms regularly
The understanding of the immune system has changed drastically in the last decade (62). A homeostatic paradigm of immunity is already accepted by a significant part of the scientific community, and new ideas, such as disease tolerance (9), add interesting perspectives to the field. Accordingly, recent findings suggest the immune system also maintain virus–host interactions (63)
Although great advances have been made in interpreting the roles of immunity from a homeostatic perspective unbiased by pathogens
thorough research and thinking are still needed
The complexity of the immune system is only matched by its ability to sustain greater complexity
As the immune system role in supporting host–microbiota interactions was consolidated
scientists now turn to the role of the immune system in other biological processes or systems
The field of neuroimmunology shows promise
as the immune and nervous systems seem intimately related in function
Pain is a connecting point between neurology and immunology where sensing and interactive properties of nervous and immune systems converge
pain translates into a great opportunity for research
and MT contributed with both intellectual and written information
All authors agreed on the final version of the manuscript and are accountable for its contents
The authors would like to thank Caio Tavares Fagundes
and Nadia Neto for comments on the manuscript