Microbiota are thought to influence the development and progression of inflammatory bowel disease (IBD), but determining generalizable effects of microbiota on IBD etiology requires larger-scale functional analyses. We colonized germ-free mice with intestinal microbiotas from 30 healthy and IBD donors and determined the homeostatic intestinal T cell response to each microbiota. Compared to microbiotas from healthy donors, transfer of IBD microbiotas into germ-free mice increased numbers of intestinal Th17 cells and Th2 cells and decreased numbers of RORγt+ Treg cells. Colonization with IBD microbiotas exacerbated disease in a model where colitis is induced upon transfer of naive T cells into Rag1-/- mice. The proportions of Th17 and RORγt+ Treg cells induced by each microbiota were predictive of human disease status and accounted for disease severity in the Rag1-/- colitis model. Thus, an impact on intestinal Th17 and RORγt+ Treg cell compartments emerges as a unifying feature of IBD microbiotas, suggesting a general mechanism for microbial contribution to IBD pathogenesis.

中文翻译：

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来自炎症性肠病患者的微生物群改变肠道 Th17 和 RORγt+ 调节性 T 细胞的平衡并加剧小鼠的结肠炎。

微生物群被认为会影响炎症性肠病 (IBD) 的发展和进展，但确定微生物群对 IBD 病因的普遍影响需要更大规模的功能分析。我们用来自 30 名健康和 IBD 供体的肠道微生物群定殖无菌小鼠，并确定了对每个微生物群的稳态肠道 T 细胞反应。与来自健康供体的微生物群相比，将 IBD 微生物群转移到无菌小鼠体内会增加肠道 Th17 细胞和 Th2 细胞的数量，并减少 RORγt+ Treg 细胞的数量。在将幼稚 T 细胞转移到 Rag1-/- 小鼠后诱导结肠炎的模型中，IBD 微生物群的定植加剧了疾病。每个微生物群诱导的 Th17 和 RORγt+ Treg 细胞的比例可预测人类疾病状态，并解释 Rag1-/- 结肠炎模型中的疾病严重程度。因此，对肠道 Th17 和 RORγt+ Treg 细胞区室的影响成为 IBD 微生物群的统一特征，表明微生物对 IBD 发病机制的贡献的一般机制。