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Review
. 2007 Apr 21;13(15):2145-9.
doi: 10.3748/wjg.v13.i15.2145.

Recent advances in basic and clinical aspects of inflammatory bowel disease: which steps in the mucosal inflammation should we block for the treatment of inflammatory bowel disease?

Hitoshi Asakura  1 , Kenji Suzuki, Terasu Honma
Affiliations
Review

Recent advances in basic and clinical aspects of inflammatory bowel disease: which steps in the mucosal inflammation should we block for the treatment of inflammatory bowel disease?

Hitoshi Asakura et al. World J Gastroenterol. .

Abstract

There are four steps in the interaction between intestinal microbes and mucosal inflammation in genetically predisposed individuals from the viewpoints of basic and clinical aspects of inflammatory bowel disease (IBD). The first step is an interaction between intestinal microbes or their components and intestinal epithelial cells via receptors, the second step an interaction between macrophages and dendritic cells and mucosal lymphocytes, the third step an interaction between lymphocytes and vascular endothelial cells, and the fourth step an interaction between lymphocytes and granulocytes producing proinflammatory cytokines or free radicals and mucosal damage and repair. Recent therapeutic approaches for IBD aim to block these four steps in the intestinal inflammation of patients with IBD.

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Figures

Figure 1
Figure 1
Schema of the pathogenesis of Crohn’s disease. TLR: toll-like receptors; IL: interleukin; TNF: tumor necrosis factor; ECM: extracellular matrix; TGF: transforming growth factor.
Figure 2
Figure 2
Schema of the pathogenesis of ulcerative colitis. IL: interleukin; MCP: monocyte chemoattractant protein; TNF: tumor necrosis factor; APC: antigen-presenting cells; LPL: lamina propria lymphocytes; AcCD4Tcell: activated CD4Tcell; PMN: polymorphonuclear cell; ROS: reactive oxygen species; mono: monocyte; MadCAM: mucosal addressin cell adhesion molecule; VCAM: vascular cell adhesion molecule.
See this image and copyright information in PMC

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