Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and seventeen coded intestinal biopsies were examined by electron microscopy and evaluated for morphological evidence of mast cell and basophil secretion in situ. Sixty percent of the biopsies had evidence of secretion. Mast cell secretion was evident in control biopsies, many of which were obtained from uninvolved tissues of patients with inflammatory bowel disease. Biopsies of inflamed continent pouches from ulcerative colitis (UC) patients showed more mast cell secretion than noninflamed UC pouch biopsies. This evidence of mast cell secretion supports recent work that documents high constitutive levels of histamine in jejunal fluids of Crohn's disease patients and suggests a proinflammatory role for mast cells in inflammation associated with pouchitis.
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PMID:Ultrastructural evidence for piecemeal and anaphylactic degranulation of human gut mucosal mast cells in vivo. 148 68

Inflammatory mediators from intestinal mast cells may serve as initiators of acute and delayed inflammation. Mast cell histamine release was measured in 19 patients with inflammatory bowel diseases using gut mast cells from enzymatically dispersed endoscopic forceps biopsy specimens of macroscopically inflamed and normal tissue. Mast cells and corresponding basophils were challenged with anti-IgE, anti-IgG, subclass anti-IgG4, and formyl-methionyl-leucyl-phenylalanine (FMLP) and results were compared with those from nine patient control subjects. The mast cell count in patients with ulcerative colitis was increased compared with that in control subjects and patients with Crohn's disease, and the mast cell count obtained from inflamed tissue was greater than that of normal tissue. The study also shows the heterogeneity of the responsiveness of the histamine releasing cells to various secretagogues. Thus, mast cells released 0.4 (0.0-2.0) (median (range)) ng histamine per sample at anti-IgE challenge, and basophils were also anti-IgE responsive. In contrast, mast cells did not respond to FMLP but the corresponding basophils did. Gut mast cells released 0.3 (0.0-1.0) (median (range)) ng histamine per sample at anti-IgG4 challenge; however, the corresponding basophils did not respond to anti-IgG4. In addition, the anti-IgG4 mediated histamine release was primarily confined to patients with inflammatory bowel disease. This study substantiates previous histopathological findings that mast cells may play a functional role in the inflammatory process of inflammatory bowel diseases and provides evidence for a possible role of subclass IgG4 as a reaginic antibody.
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PMID:Histamine release from gut mast cells from patients with inflammatory bowel diseases. 169 60

Intestinal mast cells are thought to contribute to the mucosal inflammation in ulcerative colitis and Crohn's disease through release of inflammatory mediators. Since sulfasalazine and its metabolite 5-aminosalicylic acid are effective therapeutic agents in inflammatory bowel disease and have been shown to inhibit generation of inflammatory products in other cells, we examined the effect of these agents in vitro on human intestinal mast cell mediator release. Sulfasalazine (5 x 10(-4)-10(-3) M) was found to significantly enhance goat anti-human IgE-induced histamine release from intestinal mast cells, which is the same response as seen in human blood basophils, whereas its metabolite 5-aminosalicylic acid was an effective inhibitor of stimulated histamine release in both mast cells and basophils. 5-Aminosalicylic acid also inhibited production of prostaglandin D2 by the stimulated intestinal mast cells. Sulfasalazine alone, without immunologic stimulation, did not induce histamine release from mast cells or basophils, but the enhancement of ongoing mast cell activation by sulfasalazine may explain some cases of adverse reactions to the drug. The inhibition of mast cell histamine release and prostaglandin generation by 5-aminosalicylic acid demonstrates a potential therapeutic modality of this agent.
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PMID:Modulation of mediator release from human intestinal mast cells by sulfasalazine and 5-aminosalicylic acid. 170 70

Biopsies from actively inflamed areas of terminal ileum or colon in children with Crohn's disease were examined both for lamina propria mast cell density and histamine content. These were reduced in comparison with those of normal controls. The release of histamine from biopsies of inflamed tissue did not differ greatly from that of normal tissue, either spontaneously or after receiving an antihuman IgE challenge.
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PMID:Lamina propria mast cells in biopsies from children with Crohn's disease. 242 Aug 32

The distribution and concentration of human T (tryptase-positive, chymase-negative) and TC (tryptase-positive, chymase-positive) mast cells were examined in Carnoy's-fixed specimens of the gastrointestinal tract of normal individuals, patients with inflammatory bowel diseases, and patients with immunodeficiency disorders. In normal specimens, T mast cells predominated in the mucosa (89%), with a mean concentration of 17,850 +/- 4,998 per mm3 (+/- SD, n = 16), whereas TC mast cells predominated in the submucosa (90%) with a mean concentration of 7,516 +/- 1,227 per mm3 (+/- SD, n = 16). The concentrations of T and TC mast cells in specimens of ileum from five patients with active Crohn's disease and of colon from three patients with active ulcerative colitis were not significantly different (p greater than 0.4) from normal values. Three patients with combined immunodeficiency disorders demonstrated a marked decrease in the concentration of the T mast cells in the intestinal mucosa, to 540 +/- 630, and a corresponding decrease in the percentage of T mast cells to 9%. Concentrations of TC mast cells were unchanged, both in the mucosa and in the submucosa. In three patients with acquired immunodeficiency syndrome, a similar deficiency of the T mast cell type was observed in the ileal mucosa, with a mean concentration of 788 +/- 534 T mast cells per mm3, but not in the appendiceal and colonic mucosa of one of the three patients. These findings indicate a role for functional T lymphocytes in the development of the T mast cell type in humans, and suggest divergent pathways for development of T and TC mast cells.
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PMID:Deficiency of the tryptase-positive, chymase-negative mast cell type in gastrointestinal mucosa of patients with defective T lymphocyte function. 329 46

IgE production by peripheral blood lymphocytes (PBL) and rectal mucosal biopsies in vitro has been examined in patients with ulcerative colitis (UC) and Crohn's disease (CD). The degranulation of peripheral blood basophils to food antigens has also been investigated in these patients. Mitogen-induced IgE production was reduced in patients with UC, but enhanced in PBL cultures from patients with CD. Increased numbers of basophils degranulated in the presence of cows' milk in UC patients, but normal responses occurred in patients with CD. This evidence supports the suggested role of IgE-mediated mechanisms involving mast cell/basophil interactions in the pathogenesis of inflammatory bowel disease.
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PMID:In vitro IgE production by peripheral blood lymphocytes and rectal mucosal biopsies and antigen-induced basophil degranulation in patients with inflammatory bowel disease. 376 55

The effector function of eosinophils is studied in experimental models, emphasizing the prominent role played by antibodies among which IgE, and also the activation of the cytotoxic activity by mast cell-derived ECF. A tetrapeptides. The demonstration of the cytolytic effect of basic proteins present in eosinophil granules allows to clarify this mechanism on a molecular basis. Eosinophil effector function is then envisaged in various clinical situations. In pulmonary eosinophilias, a relation appears between the detection of proteins released by eosinophils and the tissue damage. Eosinophils seem also to be implied in the inflammatory process characteristic of endomyocardial disease or in Crohn's disease. Whereas they were first considered as beneficial cells for the host, the eosinophil granulocytes may therefore express according to the targets, a dual either beneficial or nocious function.
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PMID:[Effector functions of the polynuclear eosinophil]. 622 42

Histamine exhibits various biological effects in inflammatory and immunological reactions. To further define its potential role in allergic enteropathy and inflammatory bowel disease, both gut mucosal histamine levels and histamine release from endoscopic biopsy samples were measured. Tissue histamine content resulted from addition of the released amount of histamine and the remaining part of tissue histamine. The results demonstrate highly elevated mucosal histamine levels of the large intestine in allergic enteropathy. In inflammatory bowel disease histamine content and secretion were found to be significantly increased particularly in affected mucosa of Crohn's disease and ulcerative colitis than in unaffected tissue or in healthy controls. These findings give strong evidence that mast cell mediators like histamine play a role in the pathogenesis of these diseases. Mucosal histamine is thus concluded to contribute to the immuno-inflammatory reactions of the intestine found in these disease states and to reflect the degree of colonic inflammation in Crohn's disease and ulcerative colitis.
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PMID:Mucosal histamine content and histamine secretion in Crohn's disease, ulcerative colitis and allergic enteropathy. 754 99

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 micrograms/ml of colon or small bowel-derived murine ECAC or control kidney protein, or 1 microgram/ml goat anti-human IgE positive control for 30 min at 37 degrees 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.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal mast cell responses in idiopathic inflammatory bowel disease. Histamine release from human intestinal mast cells in response to gut epithelial proteins. 768 62

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/mm2) as compared to controls (258 +/- 27/mm2), 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/mm2, versus 206 +/- 18/mm2 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.
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PMID:Quantitative assessment of intestinal eosinophils and mast cells in inflammatory bowel disease. 883 15


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