Abstract

Objective To establish mice colitis model induced by dextran sulfate sodium (DSS) and analyze its immune profile. Methods 4% DSS was given to BALB/c mice for 9 days to establish acute colitis model. Drinking water without DSS was given in the following 7 days to establish recovery colitis model. Weight loss and hematochezia were monitored daily. The histological appearance of the colon and the number, phenotypes, and cytokine production of lymphocytes were evaluated. Results The total lymphocyte number [spleen: (90.1±15.2)×106 vs. (49.8±17.1)×106, P<0.01; MLN: (15.9±3.0)×106 vs. (5.5±2.2)×106, P<0.05] and the production of IL-2 [spleen: (3.9±0.7) ng/ml vs. (1.3±0.2) ng/ml, P<0.01; colonic lamina propria (CLP): (41.7±8.3) ng/ml vs. (2.0±0.2) ng/ml, P<0.01] and interferon (IFN)-γ [spleen: (12.7±1.7) ng/ml vs. (6.8±0.8) ng/ml, P<0.01; CLP: (47.9±6.2) ng/ml vs. (17.2±3.3) ng/ml, P<0.01] were decreased, while the ratio of CD4+ /CD8+ cells [spleen: 1.7±0.2 vs. 2.8±0.7, P<0.01; MLN: 2.5±0.5 vs. 4.0±0.5, P<0.01] was increased in acute DSS colitis. However, the production of IL-4 and IL-10 was unchanged. In addition, DSS inhibited the proliferation, while promoted the apoptosis of lymphocytes. Conclusion DSS caused the imbalance of Th1/Th2 response and altered the local and systematic immune state in mice. Key words: Inflammatory bowel disease; Ulcerative colitis; Dextran sulfate sodium; Cytokine

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