Murine
genital tract infection with Neisseria gonorrhoeae has previously been found to induce
IL-17 which is important in both recruitment of neutrophils and prompt clearance of the
infection. As
IL-22 is another Th17-related
cytokine that has been implicated in the immune responses in several
infection models, we investigated its role in vaginal gonococcal
infection of mice. Production of
IL-22 was observed in response to stimulation with N. gonorrhoeae in both mouse splenic mononuclear cells and vaginal tissue explants cultured ex vivo. Tissue from mice genetically deficient in
IL-22 showed diminished production of
IL-6 and the
CXC chemokine KC in response to N. gonorrhoeae, whereas
IL-17 and the
chemokines LIX and MIP-2α were produced to the same extent as in wild-type tissue. IL-22-deficient mice were unexpectedly resistant to
genital tract infection with N. gonorrhoeaein vivo, but showed no change in the influx of neutrophils to the site of
infection. These results reveal divergent roles for
IL-17 and
IL-22 in response to gonococcal
infection.