Effects of IL-13 on murine listeriosis

Abstract

Acquired resistance against Listeria monocytogenes is a typical T helper (T(h)) 1 dominated immune response, whereas T(h)2 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 T(h)2 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-γ-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-γ 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-γ in IL-13-induced antilisterial resistance.