| Aims:To study effects of Helicobacter pylori (Hp) infection on dextran sulfate sodium (DSS)-induced acute and chronic colitis of mice, and investigation on possible immunologic mechanism of this effect.Methods:Sixty C57BL/6 mice were randomly divided into 6 group, including Control group, Hp group (infected with H. pylori SS1 strain), Acute group (drinking of 3% DSS for 7 days), Chronic group (drinking of 2% DSS for 5 days, followed by regular water for 6 days, and repeating 3 cycles), (Hp+Acute) group (inducing acute colitis after infected with Hp for 6 weeks), (Hp+Chronic) group (inducing chronic colitis after infected with Hp for 6 weeks). Weight, stool consistency and bleeding of mice were observed every day. Entire colon was measured and fixed for histological analysis. Disease activity index (DAI) and histopathological score were calculated. The expression level of interferon y (IFN-y), interleukin 12 (IL-12), tumor necrosis factor a (TFN-a), interleukin 6 (IL-6), interleukin 17 (IL-17), interleukin 4 (IL-4) and interleukin 10 (IL-10) in colon were evaluated by ELISA and Real-time PCR.Results:Compared with acute group and chronic group, clinical symptoms, including loss of weight, diarrhea and bleeding, were significantly relieved in colitis of mice (Hp+Acute) group and (Hp+Chronic) group. And DAI and histopathological scores in (Hp+Acute) group and (Hp+Chronic) group were significantly lower than acute group and Chronic group, respectively (P<0.05). Compared with the Control group in the colon, expression level of IFN-y, TNF-a, IL-6 and IL-17 in Acute group and Chronic group significantly increased (P<0.01) and IL-4 significantly decreased in Chronic group. In Hp-infected (Hp+Acute) group and (Hp+Chronic) group mice, level of IFN-γ, TNF-α and IL-6 and IL-17 were lower (P<0.01) and IL-4 was higher than in Acute group and Chronic group (P<0.05). Expression level of IL-10 was not significant difference between colitis model group and Control group.Conclusions:Helicobacter pylori infection can reduce clinical symptoms and pathologic damage in colon of DSS-induced acute and chronic colitis of mice. Hp infection plays protective role in development of UC. And possible protective mechanism is that Hp may regulate Thl/Th2/Thl7 cell-mediated immune response to reduce intestinal mucosal inflammation.Aims:To determine protective mechanism of Helicobacter pylori (Hp) on ulcerative colitis (UC), effects of Hp infection on intestinal microbiota in dextean sulfate sodium (DSS)-induced acute and chronic colitis of mice were explored.Methods:Sixty C57BL/6 mice were randomly divided into 6 group, including Control group, Hp group (infected with H. pylori SS1 strain), Acute group (drinking of 3% DSS for 7 days), Chronic group (drinking of 2% DSS for 5 days, followed by regular water for 6 days, and repeating 3 cycles), (Hp+Acute) group (inducing acute colitis after infected with Hp for 6 weeks), (Hp+Chronic) group (inducing chronic colitis after infected with Hp for 6 weeks). Bacteroides fragilis Group, Clostridium coccoides Subgroup, Clostridium leptum Subgroup, Enterobacteria, Bacteroides-Prevotella Group, Lactobacillus Group and Helicobacter pylori were detected in gastric mucosa, colonic mucosa and stool sample by quantitative (qt) real time PCR using 16SrDNA primers.Results:(1) Helicobacter pylori in gastric mucosa of Hp group mice was significantly higher than Control group (P=0.000). And other gastric bacteria, fecal flora and colonic mucosa-associated bacteria did not change (P>0.05). (2) In Acute group, Bacteroides fragilis Group was lower (P=0.038) and Enterobacteria was higher (.P=0.049) than Control group by detecting stool sample. Bacteroides fragilis Group, Enterobacteria, Lactobacillus Group in colonic mucosa of Acute group were significantly decreased (P<0.05). And in Chronic group mice, only Enterobacteria in fecal samples was significantly increased (P=0.029) and Enterobacteria and Lactobacillus Group in colonic mucosa were increased significantly (P<0.05). (3) Enterobacteria and Lactobacillus Group in colonic mucosa of (Hp+Acute) group mice were significantly higher than Acute colitis of mice (P<0.05). Compared with Chronic group, Bacteroides fragilis Group and Enterobacteriar were significantly lower (P<0.05) in colonic mucosa of (Hp+Chronic) group mice. And Lactobacillus Group did not significantly change. Whereas, fecal flora in (Hp+Acute) group and (Hp+Chronic) group mice did not vary, compared with Acute group and Chronic group (P>0.05).Conclusions:There is close association between development of acute and chronic colitis and intestinal microbiota. The possible protective mechanism of Hp infection on development of UC is that Hp may influence changes of colonic mucosa-associated bacteria, rather than fecal microflora. |
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