[Effects of Faecalibacterium prausnitzii supernatant on Th17 cell and IL-17A in dextran sulfate sodium-induced ulcerative colitis mice].

To explore the protective and therapeutic effects of Faecalibacterium prausnitzii (Fp) supernatant on ulcerative colitis (UC) in mice induced by dextran sulfate sodium (DSS) and the underlying mechanisms. Forty male mice were randomly divided into a control group, a model group, a treatment group and a prevention group (n=10 in each group). The colorectal histopathologic damage score (HDS) were calculated; the proportion of helper T cell (Th17) in mononuclear cells (MNC) in spleen, the levels of IL-17A and IL-6 in plasma were detected; the mRNA levels of transcription factor retinoic acid-related orphan receptor-γt (ROR-γt), interleukin (IL)-17A and IL-6 in colon mucosa tissues were also determined. Compared with the model group, the colon HDS in the treatment group and the prevention group were significantly decreased (both P<0.05), but there was no significant difference in the treatment group and the prevention group (P>0.05). The proportion of Th17 cells in spleen in the treatment group and the prevention group was also remarkably lower than that in the model group (both P<0.01). The levels of IL-17A and IL-6 in plasma in the treatment group were significantly lower than those in the model group (both P<0.05). The mRNA expression of ROR-γt, IL-17A and IL-6 in the colon mucosa tissues in the treatment group were remarkably lower than those in the model group (all P<0.05). But there was no statistic difference in the level of IL-6 in the plasma and the colon mucosa tissues between the prevention group and the model group (P>0.05). Fp supernatant has protective and therapeutic effects on ulcerative colitis in mice induced by DSS, which might be mediated by decrease of Th17 and IL-17A levels in the plasma and the colon mucosa tissues. Fp supernatant also can decrease mice colitis by reducing IL-6 levels.目的：探讨普拉梭菌(Faecalibacterium prausnitzii，Fp)上清对葡聚糖酸钠(dextran sulfate sodium，DSS)诱导的小鼠溃疡性结肠炎的预防和治疗作用及机制。方法：40只雄性C57BL/6J小鼠随机分为对照组、模型组、治疗组、预防组，每组10只。观察各组小鼠的结肠组织病理学评分，计算脾Th17细胞占单核细胞比例；检测外周血浆白细胞介素-17A(interleukin-17A，IL-17A)和IL-6水平，以及结肠黏膜组织转录因子维甲酸相关孤儿核受体-γt(transcription factor retinoic acid-related orphan receptor-γt，ROR-γt)，IL-17A和IL-6的mRNA表达情况。结果：治疗组和预防组小鼠结肠组织病理损伤较模型组轻，其病理组织学评分较模型组均明显下降(均P<0.05)，预防组和治疗组之间差异无统计学意义(P>0.05)；治疗组和预防组脾辅助性T细胞(helper T cell，Th17)比例较模型组均明显下降(均P<0.01)；治疗组血浆IL-17A和IL-6水平也较模型组均明显降低(均P<0.05)，结肠组织ROR-γt，IL-17A和IL-6的mRNA表达均明显低于模型组(均P<0.05)，但预防组血浆IL-6水平和结肠组织IL-6 mRNA表达与模型组差异无明显统计学意义(均P>0.05)。结论：Fp上清可预防和治疗DSS所致的小鼠结肠炎，其机制可能为抑制脾和肠道Th17细胞的生成，减少外周血和结肠组织炎性细胞因子IL-17A分泌；Fp上清可通过降低IL-6水平来治疗结肠炎。.