首页> 外文期刊>Cell Host & Microbe >A Single Strain of Clostridium butyricum Induces Intestinal IL-10-Producing Macrophages to Suppress Acute Experimental Colitis in Mice
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A Single Strain of Clostridium butyricum Induces Intestinal IL-10-Producing Macrophages to Suppress Acute Experimental Colitis in Mice

机译:一株丁酸梭菌诱导肠道IL-10产生巨噬细胞,以抑制小鼠急性实验性结肠炎。

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摘要

Imbalance in gut bacterial composition provokes host proinflammatory responses causing diseases such as colitis. Colonization with a mixture of Clostridium species from clusters IV and XlVa was shown to suppress colitis through the induction of IL-10-producing regulatory T (Treg) cells. We demonstrate that a distinct Clostridium strain from cluster I, Clostridium butyricum [CB), prevents acute experimental colitis in mice through induction of IL-10, an anti-inflammatory cytokine. However, while CB treatment had no effect on IL-10 production by T cells, IL-10-producing F4/80+CD11 b+CD11 cint macrophages accumulated in the inflamed mucosa after CB treatment. CB directly triggered IL-10 production by intestinal macrophages in inflamed mucosa via the TLR2/MyD88 pathway. The colitis-preventing effect of CB was negated in macro-phage-specific IL-10-deficient mice, suggesting that induction of IL-10 by intestinal macrophages is crucial for the probiotic action of CB. Collectively, CB promotes IL-10 production by intestinal macrophages in inflamed mucosa, thereby preventing experimental colitis in mice.
机译:肠道细菌组成的失衡会激发宿主的促炎反应,从而引起疾病,例如结肠炎。用来自簇IV和XIVa的梭状芽孢杆菌属物种的混合物定殖可通过诱导产生IL-10的调节性T(Treg)细胞来抑制结肠炎。我们证明从群集I,丁酸梭菌[CB),不同的梭菌菌株通过诱导IL-10,一种抗炎细胞因子,在小鼠中预防急性实验性结肠炎。然而,尽管CB治疗对T细胞产生IL-10没有影响,但是在CB治疗后,产生IL-10的F4 / 80 + CD11b + CD11 cint巨噬细胞积聚在发炎的粘膜中。 CB通过TLR2 / MyD88途径直接触发发炎的粘膜中的肠道巨噬细胞产生IL-10。在巨噬细胞特异性IL-10-缺陷型小鼠中,CB的预防结肠炎作用无效,这表明肠道巨噬细胞诱导IL-10对于CB的益生作用至关重要。 CB集体促进发炎的粘膜中肠道巨噬细胞产生IL-10,从而预防小鼠实验性结肠炎。

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