Review
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 1, 2004; 10(3): 309-318
Published online Feb 1, 2004. doi: 10.3748/wjg.v10.i3.309
Key role of mast cells and their major secretory products in inflammatory bowel disease
Shao-Heng He
Shao-Heng He, Allergy and Inflammation Research Institute, Medical College, Shantou University, Shantou 515031, Guangdong Province, China
Author contributions: All authors contributed equally to the work.
Supported by the Li Ka Shing Foundation, Hong Kong, China, No. C0200001 and the Planned Science and Technology Project of Guangdong Province, China, No. 2003B31502
Correspondence to: Professor Shao-Heng He, Allergy and Inflammation Research Institute, Medical College, Shantou University 22 Xin-Ling Road, Shantou 515031, Guangdong Province, China. shoahenghe@hotmail.com
Telephone: +86-754-8900405 Fax: +86-754-8900192
Received: December 23, 2003
Revised: January 4, 2004
Accepted: January 11, 2004
Published online: February 1, 2004
Abstract

Historically, mast cells were known as a key cell type involved in type I hypersensitivity. Until last two decades, this cell type was recognized to be widely involved in a number of non-allergic diseases including inflammatory bowel disease (IBD). Markedly increased numbers of mast cells were observed in the mucosa of the ileum and colon of patients with IBD, which was accompanied by great changes of the content in mast cells such as dramatically increased expression of TNF-α, IL-16 and substance P. The evidence of mast cell degranulation was found in the wall of intestine from patients with IBD with immunohistochemistry technique. The highly elevated histamine and tryptase levels were detected in mucosa of patients with IBD, strongly suggesting that mast cell degranulation is involved in the pathogenesis of IBD. However, little is known of the actions of histamine, tryptase, chymase and carboxypeptidase in IBD. Over the last decade, heparin has been used to treat IBD in clinical practice. The low molecular weight heparin (LMWH) was effective as adjuvant therapy, and the patients showed good clinical and laboratory response with no serious adverse effects. The roles of PGD2, LTC4, PAF and mast cell cytokines in IBD were also discussed. Recently, a series of experiments with dispersed colon mast cells suggested there should be at least two pathways in man for mast cells to amplify their own activation-degranulation signals in an autocrine or paracrine manner. The hypothesis is that mast cell secretogogues induce mast cell degranulation, release histamine, then stimulate the adjacent mast cells or positively feedback to further stimulate its host mast cells through H1 receptor. Whereas released tryptase acts similarly to histamine, but activates mast cells through its receptor PAR-2. The connections between current anti-IBD therapies or potential therapies for IBD with mast cells were discussed, implicating further that mast cell is a key cell type that is involved in the pathogenesis of IBD. In conclusion, while pathogenesis of IBD remains unclear, the key role of mast cells in this group of diseases demonstrated in the current review implicates strongly that IBD is a mast cell associated disease. Therefore, close attentions should be paid to the role of mast cells in IBD.

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