Involvement of Interferon- and Tumor Necrosis Factor- in Host Defense against Rhodococcus equi

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Abstract
Rhodococcus equi is a facultative, intracellular, gram-positive coccobacillus increasingly reported as an opportunistic pathogen in AIDS patients. In vitro, splenic cells of noninfected euthymic mice produced tumor necrosis factor-α (TNFα) in greater amounts when incubated with live R. equi rather than with killed bacteria. In vivo, interferon-γ (IFN-γ) and TNFa serum levels of infected euthymic mice remained below the level of detectability. Treatment of infected nude mice, which developed chronic infection, with discontinuous injections of IFN-γTNFα, or both did not decrease bacterial colony-forming units in liver, spleen, or lungs. However, treatment of infected euthymic mice, which cured a R. equi inoculum within 3 weeks, with anti-IFN-γ or anti-TNFα antibodies (or both) significantly increased tissue colony counts. These data argue that, in this murine model, endogenous IFN-γ, and TNFα are involved in the cell-mediated immunologic response against R. equi infection.

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