Active inflammatory bowel disease (IBD) often coincides with increases of Ruminococcus gnavus, a gut microbe found in nearly everyone. It was not known how, or if, this correlation contributed to disease. We investigated clinical isolates of R. gnavus to identify molecular mechanisms that would link R. gnavus to inflammation. Here, we show that only some isolates of R. gnavus produce a capsular polysaccharide that promotes a tolerogenic immune response, whereas isolates lacking functional capsule biosynthetic genes elicit robust proinflammatory responses in vitro. Germ-free mice colonized with an isolate of R. gnavus lacking a capsule show increased measures of gut inflammation compared to those colonized with an encapsulated isolate in vivo. These observations in the context of our earlier identification of an inflammatory cell-wall polysaccharide reveal how some strains of R. gnavus could drive the inflammatory responses that characterize IBD.

活动性炎症性肠病 (IBD) 通常与齿状瘤胃球菌的增加同时发生，齿状瘤胃球菌是一种几乎存在于每个人体内的肠道微生物。目前尚不清楚这种相关性如何或是否会导致疾病。我们研究了R. gnavus的临床分离株，以确定将R. gnavus与炎症联系起来的分子机制。在这里，我们发现只有一些R. gnavus分离株产生促进耐受性免疫反应的荚膜多糖，而缺乏功能性荚膜生物合成基因的分离株在体外引发强烈的促炎症反应。与体内植入有胶囊的分离株相比，植入缺乏荚膜的R. gnavus分离株的无菌小鼠肠道炎症指标有所增加。在我们早期鉴定炎症细胞壁多糖的背景下，这些观察结果揭示了一些R. gnavus菌株如何驱动 IBD 特征的炎症反应。