title: Eimeria tenella: interleukin 17 contributes to host immunopathology in the gut during experimental infection.
abstract: Although IL-17 is a key factor in Th17 lineage host responses and plays critical roles in immunological control of a variety of infectious diseases, the contribution of IL-17 to immune function during Eimeria tenella infection is unknown. In the present study, we used an experimental E. tenella infection model to clarify the role of Th17-associated response in the resulting immune response by quantitative real-time PCR assays. We observed robust production of STAT-3 (the transcription factors), IL-1β, IL-6 and IL-17 in cecal intraepithelial lymphocytes during the early infection, peaking at 6h p.i. and declining thereafter. The expression of TGF-β was moderately upregulated and had 2 peaks at 6 and 72h p.i. during the early infection. To further investigate the role of chIL-17 during the infection, we treated the infected chickens with IL-17 and its neutralized antibody. As a result, the reduced fecal oocyst shedding and cecal lesion scores, but enhanced body weight gains were observed in IL-17 neutralized chickens. The results of histopathology showed that the neutrophils recruitment diminished and the parasite burden in IL-17 neutralized chickens decreased. These results may be due to the significant decrease in the production of IL-17, IL-6 and TGF-β, but enhanced IL-12 and IFN-γ expression in IL-17 neutralized chickens. The converse results were shown in IL-17 treated infected-chickens in which chickens showed increased fecal oocyst shedding, exacerbated lesion scores, and reduced body weight gains. These results suggested that chicken IL-17 might mediate E. tenella - induced immunopathology during the infection.
authors.affiliation: National Animal Protozoa Laboratory, College of Veterinary Medicine, China Agricultural University, Haidian District, Beijing 100193, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Renqiang
authors.initials: R
authors.lastname: Liu
authors.forename: Meng
authors.initials: M
authors.lastname: Song
authors.forename: Yanxin
authors.initials: Y
authors.lastname: Hu
authors.forename: Baoliang
authors.initials: B
authors.lastname: Pan
authors.forename: Jianping
authors.initials: J
authors.lastname: Cai
authors.forename: Ming
authors.initials: M
authors.lastname: Wang
mesh_terms: D000818:Animals; D000913:Antibodies, Protozoan / Q000276:immunology; D002432:Cecum / Q000473:pathology; D002645:Chickens / Q000469:parasitology*; D003001:Cloning, Molecular; D003048:Coccidiosis / Q000276:immunology / Q000473:pathology / Q000662:veterinary*; D016786:Eimeria tenella / Q000276:immunology* / Q000472:pathogenicity; D005243:Feces / Q000469:parasitology; D005786:Gene Expression Regulation; D007371:Interferon-gamma / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology; D016133:Polymerase Chain Reaction / Q000662:veterinary; D011201:Poultry Diseases / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D011817:Rabbits; D011994:Recombinant Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000235:genetics / Q000378:metabolism; D013047:Specific Pathogen-Free Organisms; D058504:Th17 Cells / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D015430:Weight Gain
chemical_list: D000913:Antibodies, Protozoan; D020381:Interleukin-17; D053583:Interleukin-1beta; D015850:Interleukin-6; D011994:Recombinant Proteins; D050796:STAT3 Transcription Factor; D016212:Transforming Growth Factor beta; D018664:Interleukin-12; D007371:Interferon-gamma