RÉSUMÉ
Objective To explore the therapeutic effects and the mechanisms of Faecalibacterium prausnitzii (Fp) on trinitro-benzene-sulfonic acid-induced colitis.Methods Sixty Sprague-Dawley rats were divided into healthy control group, colitis model control group, Fp pretreated group,Fp supernatant pretreated group,Fp treated group and Fp supernatant treated group.Disease activity index (DAI),histological injury of colonic tissue,the content of butyrate in feces,forkhead box protein 3 (Foxp3) regulatory T cells (Treg) in peripheral blood and spleen and the level of interlenkin (IL)-17 and IL-6 in serum were evaluated.All the data were statistical analyzed by single factor analysis of variance. Results Compared with colitis model control group, DAI significantly lowered and histological injury obviously improved in Fp pretreated group, Fp supernatant pretreated group,Fp treated group and Fp supernatant treated group.The effects of Fp pretreated group were better than those of Fp treated group and Fp supernatant pretreated group were better than Fp supernatant treated group.The concentration of butyrate in Fp pretreated group,Fp supernatant pretreated group,Fp treated group and Fp supernatant treated group was (3091.08 ±485.50) × 106 mol/L,(1714.64 ± 351.25) × 10(-8) mol/L,(2064.75 ± 295.04) × 10-6 mol/L and (1089.13±321.23) × 10-6 mol/L respectively,there was significant difference between Fp pretreated group and other groups (F=49.796,P＜0.01).The peripheral blood level of Foxp3+ Treg in Fp supernatant pretreated group was highest.The spleen level of Foxp3+ Treg in Fp pretreated group and Fp supernatant pretreated group were significantly higher than that of other groups.The serum level of IL-17 and IL-6 in Fp pretreated group,Fp supernatant pretreated group,Fp treated group and Fp supernatant treated group was significantly lower than that of colitis model group.Conclustons Fp plays a role in promoting the repair of intestinal inflammatory reaction in colitis model rats.The mechanism may be related with butyrate producing,the peripheral blood and spleen level of Foxp3+ Treg up-regulating,suppressing the secretion of proinflammatory cytokine IL-17 and IL-6.Rebuilding the balance of Treg/Th17 to reduce local intestinal inflammation.