Intestinal epithelial cells in inflammatory bowel diseases

被引:151
作者
Roda, Giulia [1 ]
Sartini, Alessandro [1 ]
Zambon, Elisabetta [1 ]
Calafiore, Andrea [1 ]
Marocchi, Margherita [1 ]
Caponi, Alessandra [1 ]
Belluzzi, Andrea [1 ]
Roda, Enrico [1 ]
机构
[1] Univ Bologna, Dept Clin Med, Gastroenterol Unit, S Orsola M Malpighi Hosp, I-40138 Bologna, Italy
关键词
Intestinal epithelial cells; Epithelial barrier; Tight junctions; Crohn's disease; Ulcerative colitis; NECROSIS-FACTOR-ALPHA; MUCOSAL BARRIER FUNCTION; CROHNS-DISEASE; ULCERATIVE-COLITIS; TIGHT JUNCTIONS; INTERFERON-GAMMA; T-CELLS; LYMPHOCYTE INTERACTIONS; IMMUNE HOMEOSTASIS; LAMINA PROPRIA;
D O I
10.3748/wjg.v16.i34.4264
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
The pathogenesis of inflammatory bowel diseases (IBDs) seems to involve a primary defect in one or more of the elements responsible for the maintenance of intestinal homeostasis and oral tolerance. The most important element is represented by the intestinal barrier, a complex system formed mostly by intestinal epithelial cells (IECs). IECs have an active role in producing mucus and regulating its composition; they provide a physical barrier capable of controlling antigen traffic through the intestinal mucosa. At the same time, they are able to play the role of non-professional antigen presenting cells, by processing and presenting antigens directly to the cells of the intestinal immune system. On the other hand, immune cells regulate epithelial growth and differentiation, producing a continuous bi-directional cross-talk within the barrier. Several alterations of the barrier function have been identified in IBD, starting from mucus features up to its components, from epithelial junctions up to the Toll-like receptors, and altered immune responses. It remains to be understood whether these defects are primary causes of epithelial damage or secondary effects. We review the possible role of the epithelial barrier and particularly describe the role of IECs in the pathogenesis of IBD. (C) 2010 Baishideng. All rights reserved.
引用
收藏
页码:4264 / 4271
页数:8
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