Acquired resistance against Listeria monocytogenes is a typical T helper (Th) 1 dominated immune response, whereas Th2
cytokines are thought to worsen
listeriosis. We investigated effects of recombinant
IL-13 (rIL-13) on the host response to L. monocytogenes in mice. Although
IL-13 has been described as a Th2
cytokine with deactivating anti-inflammatory activities, it was found to enhance antilisterial resistance. In vitro, rIL-13 increased
IL-12 p40 and p70 production by bone marrow macrophages infected with L. monocytogenes. In vivo, numbers of viable bacteria in spleens and livers were decreased
after treatment of mice with rIL-13. In addition,
granuloma formation was impaired and NK cell activity of spleen cells was enhanced. At the onset of
infection, frequencies of IL-12-producing cells were increased and numbers of IL-4- and IFN-gamma-secreting cells were diminished in rIL-13-treated mice as compared to controls. In contrast, on day 6 after
infection,
IL-12,
IL-4 and IFN-gamma levels in rIL-13-treated animals were equal to or even higher than those in controls. Although direct activation of host macrophages by
IL-13 is possible, we consider it more likely that
IL-13 acted indirectly through stimulation of
IL-12 production and inhibition of
IL-4 release early after
infection. In contrast, our data argue against an apparent role of IFN-gamma in IL-13-induced antilisterial resistance.