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首页> 外文期刊>Cell Reports >Microbiota-Regulated IL-25 Increases Eosinophil Number to Provide Protection during Clostridium difficile Infection
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Microbiota-Regulated IL-25 Increases Eosinophil Number to Provide Protection during Clostridium difficile Infection

机译：微生物群调节的IL-25可增加嗜酸性粒细胞数，在艰难梭菌感染期间提供保护

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Clostridium difficile infection (CDI) is the most common cause of hospital-acquired infection in the United States. Host susceptibility and the severity of infection are influenced by disruption of the microbiota and the immune response. However, how the microbiota regulate immune responses to mediate CDI outcome remains unclear. Here, we have investigated the role of the microbiota-linked cytokine IL-25 during infection. Intestinal IL-25 was suppressed during CDI in humans and mice. Restoration of IL-25 reduced CDI-associated mortality and tissue pathology even though equivalent levels of C. difficile bacteria and toxin remained in the gut. IL-25 protection was mediated by gut eosinophils, as demonstrated by an increase in intestinal eosinophils and a loss of IL-25 protection upon eosinophil depletion. These findings support a mechanism whereby the induction of IL-25-mediated eosinophilia can reduce host mortality during active CDI. This work may provide targets for future development of microbial or immune-based therapies.
机译：艰难梭菌感染（CDI）是美国医院获得性感染的最常见原因。宿主易感性和感染的严重程度受微生物群破坏和免疫反应的影响。但是，微生物群如何调节免疫应答以介导CDI结果尚不清楚。在这里，我们研究了微生物群相关的细胞因子IL-25在感染过程中的作用。在人类和小鼠的CDI期间，肠道IL-25被抑制。 IL-25的恢复降低了CDI相关的死亡率和组织病理学，即使肠道中仍存在同等水平的艰难梭菌细菌和毒素。肠道嗜酸性粒细胞的增加和嗜酸性粒细胞耗竭后IL-25保护的丧失证明了肠道嗜酸性粒细胞介导的IL-25保护作用。这些发现支持了一种机制，通过该机制可以诱导IL-25介导的嗜酸性粒细胞减少活性CDI期间的宿主死亡率。这项工作可能为微生物或基于免疫疗法的未来发展提供目标。

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