title: The inhibitory effect of environmental ammonia on Danio rerio LPS induced acute phase response.
abstract: Ammonia is a toxic by-product of amino acid catabolism and a common environmental pollutant that has been associated with increased disease susceptibility in fish although the mechanism is not well understood. We addressed the hypothesis that elevated environmental ammonia acts by impairing the acute phase response (APR). Specifically, we determined the impact of sub-lethal acute (24 h) and chronic (14 d) ammonia exposure on acute phase protein gene expression in zebrafish (Danio rerio) in response to a challenge with bacterial lipopolysaccharide (LPS: i.p. 10 μg/g after 24h). A panel of LPS-responsive genes (SAA, HAMP, LECT2, Hp and IL1β) were identified and evaluated by real-time quantitative PCR. Ammonia was found to impair induction of SAA, HAMP and LECT2 by 50-90%. Both short (15 min, 1h and 24h) and long-term (14 days) exposure to high environmental ammonia concentrations significantly elevated whole-body cortisol levels compared with control fish. Our results reveal for the first time that exposure to high environmental levels of ammonia suppresses the innate immune response in fish. We hypothesize that high environmental ammonia-mediated elevation of cortisol levels in zebrafish may be playing a key role in this immunosuppression, while the mechanisms involved remains to be elucidated.
authors.affiliation: Centro Interdisciplinar de Investigação Marinha e Ambiental, Porto, Portugal. fgoncalves@ciimar.up.pt
authors.forename: A F
authors.initials: AF
authors.lastname: Gonçalves
authors.forename: I
authors.initials: I
authors.lastname: Páscoa
authors.forename: J V
authors.initials: JV
authors.lastname: Neves
authors.forename: J
authors.initials: J
authors.lastname: Coimbra
authors.forename: M M
authors.initials: MM
authors.lastname: Vijayan
authors.forename: P
authors.initials: P
authors.lastname: Rodrigues
authors.forename: J M
authors.initials: JM
authors.lastname: Wilson
mesh_terms: D000210:Acute-Phase Reaction / Q000276:immunology*; D000641:Ammonia / Q000506:poisoning*; D000818:Animals; D023181:Antimicrobial Cationic Peptides / Q000235:genetics / Q000276:immunology; D002097:C-Reactive Protein / Q000235:genetics / Q000276:immunology; D004781:Environmental Exposure / Q000009:adverse effects*; D064451:Hepcidins; D006854:Hydrocortisone / Q000032:analysis; D007113:Immunity, Innate / Q000187:drug effects / Q000276:immunology; D016753:Interleukin-10 / Q000235:genetics / Q000276:immunology; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D012313:RNA / Q000737:chemistry / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000685:Serum Amyloid A Protein / Q000235:genetics / Q000276:immunology; D018709:Statistics, Nonparametric; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology; D015027:Zebrafish / Q000235:genetics / Q000276:immunology*; D029961:Zebrafish Proteins / Q000235:genetics / Q000276:immunology
chemical_list: D023181:Antimicrobial Cationic Peptides; D064451:Hepcidins; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D000685:Serum Amyloid A Protein; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D029961:Zebrafish Proteins; C545339:tlr4ba protein, zebrafish; D016753:Interleukin-10; D012313:RNA; D000641:Ammonia; D002097:C-Reactive Protein; D006854:Hydrocortisone