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.

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