The proinflammatory cytokine interleukin (IL)-17 plays important roles in various inflammatory diseases, and IL-17-producing T helper 17 cells (Th17) have received much attention. For therapy of Th17-mediated diseases, some reports have indicated the clinical efficacy of lactic acid bacteria, including Streptococcus thermophilus. In this study, we examined the mechanism for the suppressive effects of S. thermophilus ST28 on the Th17 response in murine splenocytes stimulated with transforming growth factor (TGF)-β plus IL-6. Stimulation with TGF-β plus IL-6 increased mRNA expression of IL-17 and its production in the splenocytes, but ST28 markedly suppressed both. Meanwhile, ST28 increased the mRNA expression of interferon (IFN)-γ as well as its production. Anti-IFN-γ completely cancelled the suppressive effect of ST28 on IL-17 production. From these data, it was concluded that IFN-γ induced by ST28 had an important role on the effect. A genomic DNA (10 µg/ml) from ST28 effectively suppressed IL-17 production, probably via the Toll-like receptor 9. Therefore, modulation of Th1/Th17 balance would be one of the mechanisms under which S. thermophilus ST28 exerts an anti-inflammatory effect.

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