1. Neural Adhesion Molecule Close Homolog of L1 Deficiency Exacerbates DSS-Induced Colitis in Mice
- Author
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Cheng Xiang, Ming Fan, Liang Guo, Ling-Ling Zhu, Ying Han, Dan Liu, Ming Zhao, Ming Shi, Tong Zhao, Xiaomeng Wang, and Kuiwu Wu
- Subjects
Neural adhesion molecule ,Chemistry ,medicine ,Colitis ,medicine.disease ,digestive system diseases ,Cell biology - Abstract
Background: The cell adhesion molecule CHL1, which belongs to the immunoglobulin superfamily, functions in a variety of physiological and pathological processes including neural development, tissue injury and repair. Recently, we found CHL1 was co-localized with GFAP positive cells in mouse colon tissue. Methods: Here, Colon tissues were collected from CHL1+/+ , CHL1+/- and CHL1-/- mice after dextran sodium sulfate (DSS) induced to investigate the effects of CHL1 on the development of DSS-induced colitis. Results: The data showed that CHL1 expression was increased in distal colon in a time-dependent manner after DSS-treatment. CHL1 deficiency induced more pronounced colitis features, an exacerbation of inflammation and damage to colonic tissues in DSS-induced mouse than that of wild type mouse. Moreover, CHL1-/- mice showed a remarkable increase of neutrophil and macrophage infiltration into colonic tissues, and then result in more severe damage to the intestinal epithelial cells and FITC leakage in CHL1 deficiency mice than that in WT mouse. Conclusions: Our results revealed a distinct colonic role for CHL1 in regulating DSS-induced colitis, CHL1 deficiency exacerbates DSS-induced colitis in mice, indicating that CHL1 may be an attractive therapeutic target for IBD.
- Published
- 2020