Submitted to: International Congress on Cytokines/Chemokines in Infectious Disease
Publication Type: Abstract only
Publication Acceptance Date: 11/20/1999
Publication Date: N/A
Citation: Interpretive Summary:
Technical Abstract: Coccidiosis, caused by protozoan parasites of Eimeria., impairs the intestinal tract resulting in a significant nutrient malabsorption and body weight loss. The role of intestinal lymphocytes and IFN-gamma production in protective immunity to Eimeria tenella infection was evaluated in two inbred strains of chickens (SC and TK) that display different patterns of susceptibility to coccidiosis. Oral inoculation of either chicken strain with E. tenella lead to parasite invasion of not only the intestinal cecum but also the cecal tonsils with greater fecal oocyst shedding in TK chickens. Flow cytometric analyses of cecal tonsil lymphocytes demonstrated greater numbers of CD4+ and TCR1+ cells in SC chickens and elevated numbers of CD8+ and TCR2+ cells in TK chickens following primary infection. IFN-gamma mRNA expression was significantly increased in cecal tonsil and intraepithelial lymphocytes at days 6 and 8 post-primary infection respectively in SC compared to TK chickens. While no differences were noted between cecal tonsil lymphocytes of the two strains following secondary infection, TK chickens showed elevated IFN-gamma transcript levels in intestinal intraepithelial lymphocytes at this time. Selective depletion of CD4+ but not CD8+ cecal tonsil lymphocytes in SC chickens resulted in a reduction in IFN-gamma RNA expression indicating that CD4+ cells are the primary source of production of this cytokine. Collectively, these results indicate that the production of IFN-gamma and local lymphocyte responses are under host genetic factor(s) which influence the magnitude of the host innate immunity to E. tenella.