ABSTRACT
Objective To investigate the protective effects and mechanism of Faecalibacterium prausnitzii (Fp) and its products in 2,4,6-trinitrobenzene sulfonic acid (TNBS) induced colitis rats.Methods A total of 40 Sprague-Dawley rats were divided into healthy control group,colitis model group,Fp supernatant group,Fp bacteria group and Bifidobacterium longum (B.longum) group.The rats of the later four groups were enemaed with TNBS to establish the model.At five days before and one day after modeling,the rats were gavaged with phosphate buffer saline (PBS),the supernatant of Fp,live Fp bacteria and live B.longum respectively.Rats were executed at 48 hour after modeling.The colon tissues were taken for pathology examination.The content of short-chain fatty acids (SCFA) in fecal was tested by gas chromatography.The plasma level of interleukin-10 (IL- 10),interleukin-12 ( IL-12),interleukin-17 (IL-17) and interleukin-23 (IL-23) were detected by enzyme-linked immunosorbnent assay (ELISA) and the expression of IL-17 in intestinal mucosal tissues was measured by immunohistochemistry.The data were analyzed by one way ANOVA.Results Compared with the healthy control group,the rats of colitis group suffered serious weight loss and their intestinal pathology score increased [(193.57±14) g vs (170.25±19.18) g,(1.00±0.99) vs (3.34±0.38),t=2.83 and 7.55,all P value＜0.05].The Fp supernatant group showed protective effects in terms of weight and intestinal pathology score [(187.00± 14.67) g,(2.50±0.44),t=2.1 and 2.9,all P＜0.05].Compared with healthy control group,the plasma and colon tissue IL-17 concentration of colitis model group increased (16.61 pg/ml±2.45 pg/ml vs 20.47 pg/ml± 1.45 pg/ml,0.83±0.98 vs 5.14±0.90) (all P＜0.05).Compared with the colitis model group,the plasma and colon tissue IL-17 concentration of Fp supernatant group decreased ( 17.54 pg/ml± 1.51 pg/ml and 2.86±0.69).Conclusion Fp can regulate immune response and suppress rat colonic inflammation,which may be related with the expression of IL-17.
ABSTRACT
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.