کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1905069 | 1534688 | 2012 | 8 صفحه PDF | دانلود رایگان |

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.
Research highlights
► Mast cells are prototypes of innate immune cells that can be controlled by neuronal mediators.
► In the bowel, these cells comprise different subtypes that develop in accordance to the cytokine microenvironment.
► Evidence links mast cell activity to epithelial barrier dysfunction or activation of adaptive or innate immune responses.
► Mast cells are involved in the pathogenesis of bowel disorders via the neurogenic cytokine and protease release.
► Mast cell related adjunctive therapy in these pathologies should be considered.
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1822, Issue 1, January 2012, Pages 66–73