Endogenous interleukin-12 is not required for resolution of Chlamydophila abortus (Chlamydia psittaci serotype 1) infection in mice
2001
Rio, L. del | Buendia, A.J. | Sanchez, J. | Gallego, M.C. | Caro, M.R. | Ortega, N. | Seva, J. | Pallares, F.J. | Cuello, F. | Salinas, J.
A Th1 immune response involving gamma interferon (IFN-gamma) production is required to eliminate Chlamydophila abortus infections. In this study, the role of interleukin-12 (IL-12) in protecting against C. abortus infection was investigated using IL-12-/- and wild-type (WT) C57BL/6 mice to determine the role of this Th1-promoting cytokine. IL-12-/- mice were able to eliminate the C. abortus infection in a primary infection. However, there was a delay in the clearance of bacteria when IL-12-/- mice were infected with a sublethal dose of C. abortus, the delay being associated with a lower production of IFN-gamma. The low level of IFN-gamma was essential for survival of IL-12-/- infected mice. Both WT and IL-12-/- mice developed a Th1 immune response against C. abortus infection, since they both produced IFN-gamma and immunoglobulin G2a antibody isotype. In addition, when mice were given a secondary infectious challenge with C. abortus, a protective host response which resolved the secondary infection was developed by both WT and IL-12-/- mice. The lack of IL-12 resulted in few infiltrating CD4+ T cells in the liver relative to the number in WT mice, although the number of CD8+ T cells was slightly higher. The more intense Th1 response presented by WT mice may have a pathogenic effect, as the animals showed higher morbidity after the infection. In conclusion, these results suggest that although IL-12 expedites the clearance of C. abortus infection, this cytokine is not essential for the establishment of a protective host response against the infection.
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