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Quantitative assessment of intestinal eosinophils and mast cells in inflammatory bowel disease
Author(s) -
BISCHOFF S.C.,
WEDEMEYER J.,
HERRMANN A.,
MEIER P.N.,
TRAUTWEIN C.,
CETIN Y.,
MASCHEK H.,
STOLTE M.,
GEBEL M.,
MANNS M.P.
Publication year - 1996
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1046/j.1365-2559.1996.262309.x
Subject(s) - chymase , mast cell , lamina propria , tryptase , degranulation , inflammatory bowel disease , pathology , medicine , immunohistochemistry , inflammation , ulcerative colitis , pathogenesis , colitis , immunology , disease , epithelium , receptor
Previous studies on the frequency of intestinal mast cells and eosinophils in patients with inflammatory bowel disease yielded conflicting results. In the present morphometric study, we quantified mast cells and eosinophils in the lamina propria by histological and immunohistochemical methods in 64 patients suffering from Crohn’s disease (33 cases) or ulcerative colitis (31 cases), and in 29 controls. Histological data from 206 biopsies were related to the presence of mucosal inflammation and clinical parameters. The number of eosinophils was increased in patients with inflammatory bowel conditions (mean ± SE : 331 ± 44/mm 2 ) as compared to controls (258 ± 27/mm 2 ), and was dependent on disease activity and drug treatment. Mean mast cell numbers did not differ between patients and controls. However, a reduced mast cell number was found in toluidine blue‐stained sections of actively inflamed tissue areas (143 ± 16/mm 2 , versus 206 ± 18/mm 2 in non‐inflamed tissue). Immunohistochemical studies using antibodies against the granule proteins tryptase and chymase suggest that this decrease in mast cell numbers is due to mast cell degranulation. The present data show that the number of intestinal mast cells and eosinophils is altered in patients with inflammatory bowel diseases, suggesting that both cell types are involved in the pathogenesis of chronic intestinal inflammation.