Yu Jin1, Yan Lin1, Lianjie Lin1, Yan Sun1, Changqing Zheng2. 1. Department of Gastroenterology, Shengjing Hospital of China Medical University, Shenyang 110022, People's Republic of China. 2. Department of Gastroenterology, Shengjing Hospital of China Medical University, Shenyang 110022, People's Republic of China. Electronic address: zhengchangqing88@163.com.
Abstract
AIMS: To investigate the effects of exogenous carcinoembryonic antigen related cellular adhesion molecule 1 (CEACAM1) on ulcerative colitis (UC) in a dextran sulfate sodium (DSS)-induced mouse model. MAIN METHODS: UC mice model was induced by administration of DSS in drinking water for 7days. Treatment of CEACAM1 was performed by a transrectal injection of CEACAM1 gene packed adenovirus in the mice. The severity of UC was evaluated using disease activity index and colon length. Histological changes were observed after hematoxylin and eosin staining. ELISA was used to measure secretion of pro-inflammatory cytokines in the colon tissue. The expression of mRNA and protein were detected using real-time PCR and western blotting. The effect of CEACAM1 on epithelial cell restitution was evaluated using wound-healing test in Caco-2 cells. KEY FINDINGS: CEACAM1 overexpression attenuated the symptoms of UC as evidenced by decreased DAI score, increased colon length and histopathologic score. In addition, exogenous CEACAM1 reduced the levels of inflammatory cytokines and downregulated COX-2 and iNOS expression levels. Moreover, CEACAM1 overexpression decreased colonic permeability by upregulating expression of tight junction proteins. In the in vitro study, exogenous CEACAM1 promoted proliferation and migration of Caco-2 cell. SIGNIFICANCE: Exogenous CEACAM1 effectively rescues the symptoms of UC in DSS mice through preventing inflammatory responses, improving epithelial barrier and promoting epithelial cells restitution.
AIMS: To investigate the effects of exogenous carcinoembryonic antigen related cellular adhesion molecule 1 (CEACAM1) on ulcerative colitis (UC) in a dextran sulfate sodium (DSS)-induced mouse model. MAIN METHODS: UC mice model was induced by administration of DSS in drinking water for 7days. Treatment of CEACAM1 was performed by a transrectal injection of CEACAM1 gene packed adenovirus in the mice. The severity of UC was evaluated using disease activity index and colon length. Histological changes were observed after hematoxylin and eosin staining. ELISA was used to measure secretion of pro-inflammatory cytokines in the colon tissue. The expression of mRNA and protein were detected using real-time PCR and western blotting. The effect of CEACAM1 on epithelial cell restitution was evaluated using wound-healing test in Caco-2 cells. KEY FINDINGS:CEACAM1 overexpression attenuated the symptoms of UC as evidenced by decreased DAI score, increased colon length and histopathologic score. In addition, exogenous CEACAM1 reduced the levels of inflammatory cytokines and downregulated COX-2 and iNOS expression levels. Moreover, CEACAM1 overexpression decreased colonic permeability by upregulating expression of tight junction proteins. In the in vitro study, exogenous CEACAM1 promoted proliferation and migration of Caco-2 cell. SIGNIFICANCE: Exogenous CEACAM1 effectively rescues the symptoms of UC in DSSmice through preventing inflammatory responses, improving epithelial barrier and promoting epithelial cells restitution.
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