Dexamethasone suppresses T cell-mediated immunity and enhances disease susceptibility to Eimeria mivati infection.

The effect of dexamethasone (DEX) on Eimeria mivati infection in chickens was examined. Chickens given an extended DEX treatment produced significantly higher numbers of total oocysts following primary and secondary infections with E. mivati. Chickens treated with DEX intramuscularly or orally showed lower body weight gain in E. mivati infected or uninfected chickens as compared with the untreated group. Chickens given DEX intramuscularly showed a lower number of splenic lymphocytes. Flow cytometric analysis of lymphocyte composition revealed that the percentages of splenic lymphocytes bearing CD8 (cytotoxic-suppressor T cells), gamma delta T cell receptor (TCR 1), class II major histocompatibility or surface IgM antigens in DEX-treated chickens were lower than in controls, whereas the percentages of T lymphocytes expressing CD3, CD4 (helper T cells) or alpha beta TCR antigens were significantly higher. Furthermore, concanavalin A-induced lymphoproliferation, interleukin-2 (IL-2) and gamma-interferon (gamma-IFN) production by spleen lymphocytes were generally depressed in DEX-treated chickens. IL-2 production of E. mivati-infected chickens given oral DEX was significantly lower compared with the uninfected-DEX-treated group. Uninfected chickens treated with DEX intramuscularly showed a significantly lower gamma-IFN production compared with other uninfected groups. In contrast, serum IgG levels were enhanced in DEX-treated, E. mivati-infected chickens compared with untreated, infected chickens. These results suggest that enhanced disease susceptibility to coccidiosis in DEX-treated chickens may reflect a drug-mediated immunosuppression of cell-mediated immunity.