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  • Crohn's disease  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 38 (1993), S. 1105-1112 
    ISSN: 1573-2568
    Keywords: Crohn's disease ; ulcerative colitis ; mast cells ; epithelial cell associated components ; histamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mucosal and submucosal mast cell hyperplasia is a feature of the chronic inflammatory bowel diseases—ulcerative colitis and Crohn's disease. The mast cells are often seen to be degranulated in areas of active disease, suggesting that the inflammatory mediators released from these cells contribute to the pathophysiology of these disorders. We examined the hypothesis that epithelial cell-derived proteins, intestinal epithelial cell-associated components (ECAC), interact with the mast cells of patients with chronic inflammatory bowel disease to trigger the local release of mast cell mediators. Aliquots of human intestinal mucosal mast cell suspensions obtained from surgically resected specimens of colon or small intestine (ulcerative colitis, 12; Crohn's disease, 3; histologically normal controls, 8) were incubated with 1–100 μg/ml of colon or small bowel-derived murine ECAC or control kidney protein, or 1 μg/ml goat anti-human IgE positive control for 30 min at 37°C. Supernatants were analyzed in duplicate for histamine content by fluorometric assay. The median percent total histamine released by chronic inflammatory bowel disease mast cell suspensions to colonic epithelium-derived protein (ECAC-C) was 4% histamine (range 0–20%), such that the distribution of histamine release values in inflammatory bowel disease specimens was significantly different from the distribution of values in mast cells taken from normal mucosa (median 0%,P〈0.05). The median histamine release by all chronic inflammatory bowel disease specimens was also increased in response to the ECAC preparations derived from small bowel epithelium in that a third of the inflammatory bowel disease specimens showed greater than 10% histamine release to ECAC. Normal controls did not respond to either the ECAC preparations or to the kidney protein (median 0%). Our data suggest that epithelial protein-induced release of intestinal mast cell mediators may contribute to the inflammation in these chronic gastrointestinal disorders.
    Type of Medium: Electronic Resource
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