Department of Gastroenterology, Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China.
School of Materials Science and Engineering, Central South University, Changsha, Hunan 410006, P.R. China.
Mol Med Rep. 2018 Jun;17(6):7567-7574. doi: 10.3892/mmr.2018.8833. Epub 2018 Mar 29.
Roseburia intestinalis (R. intestinalis) is one of the dominant intestinal bacterial microbiota and is decreased in patients with inflammatory bowel disease (IBD). It helps protect colonic mucosa against the development of inflammation and subsequent IBD, however its underlying mechanisms are unclear. The aim of the present study was to evaluate the anti‑inflammatory properties of R. intestinalis in vitro and in an animal model of IBD. The effects of R. intestinalis on disease activity index (DAI) scores, intestinal pathology, the expression of interleukin (IL)‑17 and the frequency of CD4+CD25+Foxp3+ regulatory T cells (Treg) were evaluated in vivo in a model of 2,4,6‑trinitrobenzenesulfonic acid solution (TNBS)‑induced colitis. Compared with the control group, TNBS‑treated mice had significantly higher secretion of IL‑17, higher DAI scores, a lower ratio of Treg, reduced colon lengths and higher histological scores for colon inflammation. The administration of R. intestinalis significantly downregulated the expression of IL‑17, increased the ratio of Treg and ameliorated the high DAI scores and the pathological signs of inflammation in the colon compared with mice treated with TNBS alone. Gene expression profiling was also used to detect the expression of IL‑17 in human IBD and healthy control specimens. To extend these findings to an in vitro model of inflammation the human colon epithelial cell line NCM460 was stimulated with lipopolysaccharide (LPS) to induce inflammation and co‑cultured with R. intestinalis and changes in IL‑17 expression were evaluated. R. intestinalis inhibited the LPS‑induced secretion of IL‑17 by NCM460 cells. In conclusion, these results demonstrate that R. intestinalis inhibits IL‑17 secretion and promotes Treg differentiation in colitis, suggesting that R. intestinalis could be of potential use in the treatment of IBD.
肠道罗斯伯里氏菌（R. intestinalis）是肠道中占主导地位的细菌菌群之一，在炎症性肠病（IBD）患者中减少。它有助于保护结肠黏膜免受炎症和随后的 IBD 发展的影响，但其潜在机制尚不清楚。本研究旨在评估 R. intestinalis 在体内和 IBD 动物模型中的抗炎特性。在 2,4,6-三硝基苯磺酸溶液（TNBS）诱导的结肠炎模型中，评估了 R. intestinalis 对疾病活动指数（DAI）评分、肠道病理学、白细胞介素（IL）-17 的表达和 CD4+CD25+Foxp3+调节性 T 细胞（Treg）频率的影响。与对照组相比，TNBS 处理的小鼠 IL-17 分泌明显升高，DAI 评分升高，Treg 比例降低，结肠长度缩短，结肠炎症组织学评分升高。与单独用 TNBS 处理的小鼠相比，R. intestinalis 的给药显著下调了 IL-17 的表达，增加了 Treg 的比例，并改善了高 DAI 评分和结肠炎症的病理征象。基因表达谱分析还用于检测人类 IBD 和健康对照标本中 IL-17 的表达。为了将这些发现扩展到炎症的体外模型，用脂多糖（LPS）刺激人结肠上皮细胞系 NCM460 以诱导炎症，并与 R. intestinalis 共培养，评估 IL-17 表达的变化。R. intestinalis 抑制了 LPS 诱导的 NCM460 细胞中 IL-17 的分泌。总之，这些结果表明 R. intestinalis 抑制了结肠炎中 IL-17 的分泌并促进了 Treg 的分化，表明 R. intestinalis 可能在 IBD 的治疗中具有潜在用途。
