| Background:Chronic inflammation and colitis in colonic mucosa is the main feature of ulcerative colitis (UC). The disease course of UC could be very long and accompany with persistent symptoms. It is hard to cure UC. UC lower the life quality of patients. Patients who have longer disease course of UC are more likely to get colon cancer. The etiology and pathogenesis of UC has been extensively studied. Various hypothesis were proposed by different researchers. But till now, none of those hypothesis is perfect. At present, scholars believe that genetic factors, immune factors, intestinal mucosa barrier function factors, environmental factors and microorganism factors might be related to UC. Since UC is considered as a autoimmune disease, immune factors seems play a important role in UC. Immune factors include autoantibodies, cytokines, adhesion molecules and toll-like receptors. In normal immune reactions, inflammation cells can protect host. In the situation of immunologic derangement, inflammation cells proliferate excessively, which cause colon damage. In UC patients, the apotosis of colon epithelial cells is accelerated, while the apotosis of colon inflammation cells is slow down.antigen in colon, ultimately causing colon damage. Adhesion molecule (AM) is a group of transmembrane glycoprotein which participate in cell adhesion, chemotaxis, lymphocyte homing. The expression of AM is not decreased after the alleviation of inflammatory in UC.It leads to a persistent damage of colon. AM includes immune globulin superfamily, selectin, integrin and CD44.CHI3L1is a chitinase glycoprotein which has a chitin binding domain without chitinase activity. CHI3L1may not only increase the adhesion but also the invasion of microgram to the colon epithelial cells. CHI3L1may also increase the level of proinflammatory cytokines include NF-κB, IL-lb, IL-5, IL-6, IL-8, IL-13and TNF-a. Thus CHI3L1may play a key role in the etiology of UC.Objectives:This study observed the amelioration of dextran sulphate sodium (DSS)-induced experimental chronic ulcer colitis in mice by Bacillus Licheniformis (B.L.) and investigated the expression of CHI3L1, IL-13and CD44in colon of chronic UC mice. Methods:1、48male BALB/c mice were randomly divided into6groups,8mice in each group. There were normal group, model group, low dose B.L. group, moderate dose B.L. group, high dose B.L. group and sulfasalazine (SASP) group.2、Model of chronic UC mice:D1-7and D15-21, mice were given4%(W/V) DSS, drinking freely; D8-14and D22-28, mice were given distilled water, drinking freely. Normal group:D1-28, distilled water, drinking freely.3、Treatment,D1-28. Normal and model treated with nothing; low dose B.L. group treated with1×107CFU/d B.L. per mouse; moderate dose B.L. group treated with1×108CFU/d B.L. per mouse; high dose B.L. group treated with1×109CFU/d B.L. per mouse; SASP group treated with0.2mg SASP per mouse.Results:1、Compared with model and low dose B.L. group, weight loss and DAI of other treated groups were better (P<0.05).2、Compared with model and low dose B.L. group, gross injury score in colonic mucosa and histopathological changes of other treated groups were significantly lower (P<0.05). And there was a negative correlation between histopathological score and the dose of B.L.. There was no difference in gross injury score in colonic mucosa and histopathological changes between model group and low dose B.L. group. 3、Compared with model and low dose B.L. group, the RNA and protein expression of CHI3L1, IL-13, CD44, NF-κB and Bcl-2in colons of mice from other treated groups were lower (P<0.05).Conclusions:1、B.L. had a preventive and therapeutic effect on DSS induced chronic UC mice. The higher dose B.L. was more effective than the low dose B.L.2The preventive and therapeutic effect of aerobic probiotic (B.L.) to UC may by inhibiting the expression of CHI3L1, IL-13, CD44, NF-κB and Bcl-2in colon tissue of chronic UC mice. |
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