Mast cells and immunoglobulin E in inflammatory bowel disease.

Abstract

It is currently thought that both ulcerative colitis and Crohn's disease may be immunologically mediated, though the exact mechanisms responsible for both initiating and maintaining these two inflammatory bowel conditions are still far from clear. In recent years, the limited role of humoral antibodies in these diseases has become increasingly apparent and interest has tended to centre upon the possibility that they are the result of a cell mediated delayed hypersensitivity type of reaction in the bowel wall. In both these diseases, however, the inflammatory lesions are of a mixed type and features of an acute and a chronic inflammatory reaction are often both present. McGovern and Archer (1957) were the first to suggest that the acute inflammatory component of ulcerative colitis was mediated by mast cells, and subsequent workers have claimed that a marked increase in intestinal mast cells is a prominent feature of inflammatory bowel disease, some noting this increase only in ulcerative colitis (McAuley and Sommers, 1961;Bercovitz and Sommers, 1966;Sommers, 1966) and others finding it to be also a feature of Crohn's disease (Hiatt and Katz, 1962 These studies were made at a time when it was not yet fully established that mast cells could react with antigen and IgE to produce an immediate hypersensitivity reaction (Stanworth, 1971). Thus the possibility exists that one of the immunological mechanisms involved in inflammatory bowel disease is an immediate hypersensitivity reaction and it was with this in mind that the mast cell and IgE-containing immunocyte populations of the normal and inflamed bowel were studied. Methods MAST CELLSA preliminary study showed that bowel obtained at necropsy was unsuitable for the demonstration of mast cells and their distribution was therefore studied in surgically resected or biopsy specimens, all of which were obtained fresh. Thirty specimens of ileum were studied of which 12 were from patients with proven Crohn's disease; the remaining 18 were considered as normal controls and were attached to right hemicolectomy specimens resected for colonic carcinoma. Mast cell distribution was also studied in 44 surgically resected colons and in 60 specimens of rectum, some surgically resected and others obtained at biopsy. Of the colonic specimens, 15 were from patients with Crohn's disease, and 14 from cases of ulcerative colitis; multiple sections were taken from 861 on 11 May 2018 by guest. Protected by copyright.

IL-15 induces mast cell migration via a pertussis toxin-sensitive receptor

“…There are no reports concerning the effects of IL-15 on other important aspects of mast cell function such as migration and degranulation. Such interactions could contribute to inflammatory conditions, including rheumatoid arthritis and inflammatory bowel disease, where there is an increase in mast cell numbers [21,26] and IL-15 concentration [26,37]. Here, we report that IL-15 is chemotactic for mBMMC and hCBMC but does not cause significant degranulation of mBMMC.…”

“…Mast cell numbers are increased in conditions such as rheumatoid arthritis [16,18], inflammatory bowel disease [21][22][23] and asthma [15]. Elevated IL-15 mRNA and protein levels are also found in rheumatoid arthritis [24,25,49] and inflammatory bowel disease [37], thereby allowing the potential for mast cells and IL-15 interactions to contribute to the inflammatory response in these conditions.…”

“…Increased expression of these factors during an inflammatory response may induce accumulation of mast cells. Increased mast cell numbers are characteristic of many inflammatory disorders including asthma [15], rheumatoid arthritis [16][17][18][19][20] and inflammatory bowel disease [21][22][23]. Interestingly, recent reports suggest that both IL-15 expression [17,[24][25][26] and mast cell density are increased in rheumatoid synovium [17,18].…”

Endogenous IGF-I and αvβ3 integrin ligands regulate increased smooth muscle growth in TNBS-induced colitis

“…Studies in mast cell-deficient mice suggest that tissue mast cells do not mediate the response of murine intestinal muscle to TNBS-induced inflammation (5). Although tissue mast cell numbers are decreased during the inflammatory response to TNBS and in Crohn's disease generally (19,22,27), an increase in mast cells in the submucosa and both circular and longitudinal smooth muscle layers is seen during the chronic, fibrotic response to TNBS and in the strictures of human Crohn's disease patients suggesting mast cells play a role in tissue fibrosis (6,23,31). During the course of chronic inflammation induced by TNBS in the mouse and in other models of colitis, a sequential pattern of immunological response is observed (1,3,4).…”

Mucosal mast cells are pivotal elements in inflammatory bowel disease that connect the dots: Stress, intestinal hyperpermeability and inflammation

“…For example, there is a wide variation in the number of MC in IBD in different reports. A few studies have shown a mild to marked increase in the number of MC in subjects with active IBD [21][22][23] . King et al [26] and other researchers reported that MC number was not different between controls and subjects with inactive IBD [24][25][26] .…”