Intestinal mast cells in gut inflammation and motility disturbances
Benedicte Y De Winter1, Rene M van den Wijngaard, Wouter J de Jonge
1Laboratory of Experimental Medicine and Pediatrics, Department of Gastroenterology, University of Antwerp, Antwerp, Belgium.
Abstract:
Mast cells may be regarded as prototypes of innate immune cells that can be controlled by neuronal mediators. Their activation has been implicated in many types of neuro-inflammatory responses, and related disturbances of gut motility, via direct or indirect mechanisms that involve several mechanisms relevant to disease pathogenesis such as changes in epithelial barrier function or activation of adaptive or innate immune responses. Here we review the evidence for the involvement of mast cells in the inflammation of the bowel wall caused by bowel manipulation that leads to motility disturbances such as postoperative gastroparesis and ileus. Also in IBD there is substantial evidence for the involvement of mast cells and a mast cell-mediated neuroimmune interaction showing an increased number and an increased degranulation of mast cells. We discuss the potential of mast cell inhibition as a bona fide drug target to relief postoperative ileus. Further research on mast cell-related therapy either by stabilizing the mast cells or by blocking specific mast cell mediators as adjunctive therapy in IBD is encouraged, bearing in mind that several drugs currently used in the treatment of IBD possess properties affecting mast cell activities. This article is part of a Special Issue entitled: Mast cells in inflammation.
Related Concept Videos
Gastrointestinal Motility Disorders
Irritable Bowel Syndrome
Irritable Bowel Syndrome I: Introduction
IBS is a chronic condition that can persist over a long period or recur frequently.
The pathogenesis of IBS involves a complex interplay of the following factors:
Altered...
Gastric Motility
Peristaltic Waves and Chyme Formation
Upon food entry, the stomach initiates...
Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists
Inflammatory Bowel Disease II: Ulcerative Colitis

