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T cells in cooperation with macrophages play an important role in resolution of primary Yersinia enterocolitica infection in mice. Previous work from this laboratory demonstrated that gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) are essential mediators of these processes. In an attempt to elucidate early mechanisms of resistance, we investigated cytokine mRNA production, including that for interleukin-1 beta (IL-1 beta), IL-2, IL-4, IL-6, IL-10, TNF-alpha, and IFN-gamma, after primary as well as secondary Y. enterocolitica infection in Yersinia-susceptible BALB/c mice and Yersinia-resistant C57BL/6 mice. In both strains of mice, proinflammatory cytokines such as IL-1 beta, IL-6, and TNF-alpha were expressed rapidly and to comparable degrees, while IFN-gamma expression was enhanced two- to eightfold in C57BL/6 mice, as revealed by semiquantitative reverse transcription PCR. Similar results were found in both mouse strains after secondary Y. enterocolitica infection. IL-2 mRNA was detected only during secondary infection and disappeared rapidly in BALB/c mice. IL-4 mRNA expression was detectable in C57BL/6 but not BALB/c mice. The levels of cytokine mRNA expression correlated closely with the number of injected bacteria. The findings reported here support the hypothesis that early and enhanced production of IFN-gamma may be associated with a state of heightened resistance against Y. enterocolitica infection.

Early gamma interferon mRNA expression is associated with resistance of mice against Yersinia enterocolitica