Consumption of human breast milk (HBM) attenuates the incidence of necrotizing enterocolitis (NEC), which remains a leading and intractable cause of mortality in preterm infants. Here, we report that this diminution correlates with alterations in the gut microbiota, particularly enrichment of Propionibacterium species. Transfaunation of microbiota from HBM-fed preterm infants or a newly identified and cultured Propionibacterium strain, P. UF1, to germfree mice conferred protection against pathogen infection and correlated with profound increases in intestinal Th17 cells. The induction of Th17 cells was dependent on bacterial dihydrolipoamide acetyltransferase (DlaT), a major protein expressed on the P. UF1 surface layer (S-layer). Binding of P. UF1 to its cognate receptor, SIGNR1, on dendritic cells resulted in the regulation of intestinal phagocytes. Importantly, transfer of P. UF1 profoundly mitigated induced NEC-like injury in neonatal mice. Together, these results mechanistically elucidate the protective effects of HBM and P. UF1–induced immunoregulation, which safeguard against proinflammatory diseases, including NEC.

中文翻译：

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共生丙酸杆菌菌株 UF1 通过 Th17 细胞调节减轻肠道炎症

食用母乳 (HBM) 可以降低坏死性小肠结肠炎 (NEC) 的发病率，而坏死性小肠结肠炎仍然是早产儿死亡的一个主要原因，也是一个棘手的原因。在这里，我们报告这种减少与肠道微生物群的改变有关，特别是丙酸杆菌物种的富集。将 HBM​​ 喂养的早产儿或新鉴定和培养的丙酸杆菌菌株 P. UF1 的微生物群转入无菌小鼠体内，可提供针对病原体感染的保护作用，并与肠道 Th17 细胞的显着增加相关。Th17 细胞的诱导依赖于细菌二氢硫辛酰胺乙酰转移酶 (DlaT)，这是 P.UF1 表面层（S 层）上表达的主要蛋白质。P.UF1 与其在树突状细胞上的同源受体 SIGNR1 的结合导致了肠道吞噬细胞的调节。重要的是，P.UF1 的转移极大地减轻了新生小鼠中诱导的 NEC 样损伤。总之，这些结果从机制上阐明了 HBM 和 P.UF1 诱导的免疫调节的保护作用，可预防包括 NEC 在内的促炎性疾病。