Intestinal Inflammation and Mucosal Barrier Function

被引:399
|
作者
Sanchez de Medina, Fermin [1 ]
Romero-Calvo, Isabel [2 ]
Mascaraque, Cristina [1 ]
Martinez-Augustin, Olga [2 ]
机构
[1] Univ Granada, Sch Pharm, Inst Invest Biosanitaria Ibs Granada, Dept Pharmacol,CIBERehd, Granada, Spain
[2] Univ Granada, Sch Pharm, Inst Invest Biosanitaria Ibs Granada, Dept Biochem & Mol Biol 2,CIBERehd, Granada, Spain
关键词
tight junction; epithelial permeability; pattern recognition receptor; inflammatory bowel disease; microbiota; TIGHT JUNCTION PERMEABILITY; DEXTRAN SULFATE SODIUM; INDUCED ACUTE COLITIS; TOLL-LIKE RECEPTORS; CROHNS-DISEASE; EPITHELIAL BARRIER; BOWEL-DISEASE; DENDRITIC CELLS; CLAUDIN-2; EXPRESSION; ULCERATIVE-COLITIS;
D O I
10.1097/MIB.0000000000000204
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Intestinal mucosal barrier function is the capacity of the intestine to provide adequate containment of luminal microorganisms and molecules while preserving the ability to absorb nutrients. The central element is the epithelial layer, which physically separates the lumen and the internal milieu and is in charge of vectorial transport of ions, nutrients, and other substances. The secretion of mucus-forming mucins, sIgA, and antimicrobial peptides reinforces the mucosal barrier on the extraepithelial side, while a variety of immune cells contributes to mucosal defense in the inner side. Thus, the mucosal barrier is of physical, biochemical, and immune nature. In addition, the microbiota may be viewed as part of this system because of the mutual influence occurring between the host and the luminal microorganisms. Alteration of the mucosal barrier function with accompanying increased permeability and/or bacterial translocation has been linked with a variety of conditions, including inflammatory bowel disease. Genetic and environmental factors may converge to evoke a defective function of the barrier, which in turn may lead to overt inflammation of the intestine as a result of an exacerbated immune reaction toward the microbiota. According to this hypothesis, inflammatory bowel disease may be both precipitated and treated by either stimulation or downregulation of the different elements of the mucosal barrier, with the outcome depending on timing, the cell type affected, and other factors. In this review, we cover briefly the elements of the barrier and their involvement in functional defects and the resulting phenotype.
引用
收藏
页码:2394 / 2404
页数:11
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