胸腺基质淋巴细胞生成素
蔷薇花
免疫学
结肠炎
炎症
炎症性肠病
医学
发病机制
外周血单个核细胞
免疫系统
生物
病理
疾病
乳酸菌
细菌
体外
生物化学
遗传学
作者
Zhaohua Shen,Changxin Zhu,Yongsheng Quan,Jinn-Moon Yang,Wei Yuan,Zhenyu Yang,Shuai Wu,Weiwei Luo,Bei Tan,Xiaoyan Wang
摘要
Background and Aim The study aims to elucidate the anti-inflammatory effect and mechanism of Roseburia intestinalis (R. intestinalis) in Crohn's disease (CD). Methods 16S-rRNA genome sequencing technique is used to detect the characteristics of intestinal microbiota in untreated CD patients and healthy controls. Then the study investigates the effects of R. intestinalis on disease activity index score, intestinal pathology, the differentiation of Treg cells, and the expressions of Thymic stromal lymphopoietin (TSLP), TGF-β and IL-10 by using TNBS colitis models. At the cellular level, the study uses LPS to stimulate Caco-2 cells to conduct inflammation models and then co-culture with R. intestinalis and detect changes of TSLP and TGF-β. The study then uses R. intestinalis to stimulate peripheral blood mononuclear cells, and the change of Treg cells was detected. Results Genome sequencing of fecal samples from untreated CD patients (n = 10) revealed decreases in the abundance and diversity of intestinal microbiota, including R. intestinalis. Moreover, R. intestinalis reduced disease activity index scores, colon shortening, intestinal mucosal epithelial injury, and mucosal lymphocyte infiltration in a colitis mice model. It suppressed intestinal inflammation by increasing Treg cell numbers and expression of the anti-inflammatory cytokines TSLP, TGF-β, and interleukin-10 (P < 0.05). R. intestinalis also increased secretion of TSLP and TGF-β in lipopolysaccharide-treated Caco-2 cells. Conclusion These findings suggest that R. intestinalis suppresses CD pathogenesis by inducing anti-inflammatory responses.
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