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)

We examined the possible involvement of mast cells in a rat model of colitis, by monitoring levels of histamine at various times after inducing inflammation with intrarectal trinitrobenzene sulfonic acid in 50% ethanol. The ability of a histamine H1 antagonist, diphenhydramine, to modify colitis was also assessed. As expected, trinitrobenzene sulfonic acid in 50% ethanol induced a sustained colitis. Myeloperoxidase levels in macroscopically damaged tissue peaked at one week, and declined thereafter. In contrast, tissue histamine levels were normal at one week, then increased in damaged tissue to approximately four times normal levels at four weeks. Indices of inflammation were markedly suppressed at one week by diphenhydramine, while tissue histamine levels were unaffected. Chronic colitis in rats is thus apparently accompanied by a local mast cell hyperplasia or influx. Moreover, antagonism of a major mast cell mediator, histamine, significantly reduces the severity of inflammation in this model.
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PMID:Role of histamine in a rat model of colitis. 884 97

To clarify the anti-gastric acid secretory mechanism of 1,6-dihydro-2-[2-(2-methylpropoxy)anilino]-6-oxo-5-pyrimidinecarbo xylic acid (CAS 98772-05-5, MAR-99), the relationship between gastric acid secretion and gastric mucosal mast cell (MMC) was studied and the effect of this compound on these parameters was examined and compared with anti-allergic drugs (mast cell stabilizers) and anti-ulcer drugs. The release of histamine from MMC cultured from bone marrow and connective tissue mast cell (CTMC) isolated from peritoneal cavity was found to be induced by the addition of ethanol (final conc. 17.5%), and the inhibitory effect on histamine release from MMC is closely associated with the anti-gastric secretory effect. That is to say, MAR-99 (10(-9)-10(-7) mol/l) inhibited histamine release from MMC induced by ethanol in a concentration-dependent manner. The action of MAR-99 on MMC was more sensitive than that of CTMC. In addition, MAR-99 (100 mg/kg i.d.) suppressed gastric acid secretion. On the other hand, anti-allergic drugs (mast cell stabilizers), such as DSCG and tranilast (both 10(-7) mol/l), markedly inhibited histamine release from CTMC induced by ethanol, but these drugs (10(-8)-10(-7) mol/l) showed only a tendency to prevent the release of histamine from MMC. Furthermore these drugs (both 100 mg/ kg i.d.) had no effects on gastric acid secretion. Equally anti-ulcer drugs, such as cetraxate, teprenone and sofalcone, had no effects on histamine release from mast cells of two types and gastric acid secretion. From these results, it was suggested that MMC is closely correlated with gastric acid secretion, and the anti-gastric secretory effect of MAR-99 may mainly contribute to prevent the degranulation of MMC.
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PMID:Anti-gastric acid secretory mechanism of 1,6-dihydro-2-[2-(2-methylpropoxy)anilino]-6-oxo-5-pyrimidinecarboxylic acid. Effect on mucosal mast cell. 887 42

The inhibitory effect of cromakalim on the mediator release from mast cells caused by antigenantibody reactions was in controversy with the specific antigen used. However, it has recently been observed that cromakalim inhibits the release of mediators from superfused tracheal and parenchymal strips or lung mast cells after passive sensitization with the IgG1 antibody. An attempt, therefore, was made to determine the inhibitory mechanisms of cromakalim on the release of mediators such as histamine and leukotriene released by the activation of enzymes during mast cell activation. Guinea pig lung mast cells were purified through enzyme digestion, rough percoll and continuous percoll density gradients. The purified mast cells were prelabeled with [3H]palmitic acid. PLD activity was assessed more directly by the production of labeled phosphatidylethanol by PLD-mediated transphosphatidylation in the presence of ethanol. In the cells labelled with [3H]myristic acid, [3H] DAG production was measured. The methyltransferase activity was assessed by measuring the incorporation of [3H]methyl moiety into phospholipids in sensitized mast cells labelled with L-[3H] methylmethionine. cAMP level was measured by radioimmunoassay. Cromakalim resulted in a decrease in the amount of histamine and leukotrienes releases by 30% in the ovalumin-induced mast cell. Cromakalim had little effect on phospholipase D activity enhanced by the activated mast cell. Cromakalim inhibited the initial increase of diacylglycerol production during mast cell activations. Cromakalim inhibited the phospholipid methylation increased in the activated mast cell. These results show that cromakalim decreases histamine release by inhibiting the initial increase of 1,2-diacylglycerol during the mast cell activation, which is mediated via the phosphatidylinositide-phospholipase C system rather than the phosphatidylcholine-phospholipase D system. Furthermore, cromakalim reduces phosphatidylcholine production by inhibiting the methyltransferase, which decreases the conversion of phosphatidylcholine into arachidonic acid and inhibits the production of leukotrienes.
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PMID:The effects of cromakalim on the mediator releases from guinea pig lung mast cell activated by specific antigen-antibody reactions. 899 65

Previous reports indicate that intestinal intraluminal ethanol increases mucosal permeability (an index of mucosal injury) and histamine release by mast cells, and that the released histamine plays a role in mediating the increased permeability. In the present study, we investigated whether reactive oxygen metabolites and their major sources (xanthine oxidase and leukocytes) were involved in these ethanol effects. In rabbits, segments of the jejunum were perfused with a control solution or with 6% ethanol. In these segments, mucosal permeability was assessed by determining jejunal clearance of i.v. administered 51Cr-ethylenediaminetetraacetate (51Cr-EDTA) and 125I-bovine serum albumin (125I-BSA), and mast cell histamine release was estimated from the histamine concentration of the gut effluent. Ethanol increased 51Cr-EDTA clearance, 125I-BSA clearance, and histamine release. These ethanol effects decreased when the animals were given superoxide dismutase plus catalase (scavenger of O2- and H2O2, respectively), allopurinol, or oxypurinol (xanthine oxidase inhibitors). Administration of a monoclonal antibody (R15.7) against leukocyte adhesion molecule, CD18, inhibited completely the ethanol-induced increased 51Cr-EDTA and 125I-BSA clearances and histamine release. These and supplementary data suggest that (a) ethanol-induced mucosal injury and mast cell histamine release are mediated primarily by leukocytes, and (b) oxy radicals, especially those generated by xanthine oxidase, mediate these ethanol effects mainly by promoting leukocyte infiltration.
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PMID:Role of xanthine oxidase-derived oxidants and leukocytes in ethanol-induced jejunal mucosal injury. 901 59

Alcohol consumption has been shown to be associated with immune suppression and immune modulation. In this study, the effects of ethanol ingestion on the host immune responses to Trichinella spiralis infection and the subsequent secretion of T-helper cell-associated cytokines were investigated in rats. At the early phase of T. spiralis infection, ethanol-fed animals showed decreased numbers of blood neutrophils and eosinophils, and a decreased secretion of interferon-gamma (IFN-gamma) by mesenteric lymph node cells, compared with pair-fed controls. Suppression of this early inflammatory response to infection in the ethanol-treated groups resulted in a slower rate of expulsion of intestinal adult worms and a higher fecundity rate for female worms, compared with pair-fed controls. A dramatic decrease in blood neutrophils in the ethanol-treated groups was also manifested on day 9 postinfection. At that time, mesenteric lymph node cells from the ethanol-treated groups secreted higher amounts of mast cell proliferation-enhancing activity, which has been shown to contain T-helper type 2-associated cytokines. At the later phase of infection (day 12 to 20 day postinfection), ethanol-treated animals contained higher numbers of blood eosinophils and secreted an increased amount of interleukin-5 and mast cell proliferation-enhancing activity, compared with pair-fed controls. Although there was a slight rise with time after infection, the level of serum corticosterone was not significantly increased in the ethanol groups. Therefore, it is not likely that the observed immune modulations caused by ethanol consumption, especially in the early phase of infection, is the effect of elevated levels of corticosterone in the circulation. The present study found that ethanol consumption suppressed the initial amount of interferon-gamma secretion and inflammatory response, and may have directly or indirectly led to an enhancement of the secretion of T-helper type 2-type cytokines later in the primary immune response to T. spiralis infection.
Alcohol Clin Exp Res 1997 Oct
PMID:Ethanol consumption suppresses cell-mediated inflammatory responses and increases T-helper type 2 cytokine secretion in Trichinella spiralis-infected rats. 934 76

The objective was to characterize changes in barrier and transport function in an experimental model of colitis, and to determine whether mast cells contribute to these changes. Colitis was induced in rats with intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS, 30 mg) in 50% ethanol. Controls received 0.9% saline or the ethanol vehicle alone. In vivo loop perfusion was used to assess colonic water flux (in microliter.cm-1.h-1) and lumen-to-blood 51Cr-labeled EDTA clearance (% administered dose) after TNBS. Myeloperoxidase (MPO) was used as an index of granulocyte influx. TNBS or its vehicle caused a marked decrease in water absorption and an increase in permeability at 4 h after administration compared with saline. Neither dexamethasone (anti-inflammatory control) nor doxantrazole (mast cell stabilizer) was able to attenuate these early changes likely caused by the vehicle. In contrast, at later times, TNBS (but not its vehicle) also increased 51Cr-EDTA permeability and decreased water absorption; both effects were significantly attenuated by dexamethasone or doxantrazole. These drugs also significantly reduced TNBS-induced MPO accumulation and release of rat mast cell protease II. We conclude that experimental colitis is associated with severe defects in intestinal transport and barrier functions and that mast cells may contribute to the pathogenesis of these changes.
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PMID:Disruption of intestinal barrier function associated with experimental colitis: possible role of mast cells. 945 91

The carboxypeptidase A-catalyzed syntheses of dipeptides from L-amino acids (Phe, Tyr, Trp, Leu and Ile) were studied in various water-miscible (acetone, acetonitrile, ethanol, methanol and 1,4-dioxane) organic solvents. The highest yield (43%) was achieved in acetonitrile with L-Phe as substrate, after a 24-h incubation. The optimal conditions of Phe-Phe synthesis in acetonitrile were determined. For maximal conversion 1.2 mM L-Phe, 1.4 mg ml-1 enzyme and about 10% water are needed in buffered aqueous acetonitrile (pH 5.5) at 30 degrees C.
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PMID:Carboxypeptidase A-catalyzed dipeptide synthesis in organic media. 986 61

Chymase is an important marker for human mast cells as well as a mediator of inflammation and matrix remodelling, but research into chymase-containing mast cell subpopulations has been hampered by the lack of reagents suitable for use with formalin-fixed tissue. A monoclonal antibody to chymase (designated CC1) was prepared by immunizing a mouse with chymase purified from human skin, fusing the splenocytes with NS-1 myeloma cells, and screening the hybridoma supernatants by ELISA with recombinant human prochymase isolated from a baculovirus expression system. This antibody bound to chymase in western blots and bound selectively to cells with the morphology and distribution of mast cells in paraffin wax sections of skin, synovium, lung, and heart. In sequential sections and with double-labelling experiments, chymase was localized to cells which contained mast cell tryptase; in contrast to previous reports, no evidence was found for its presence in endothelial cells or any other cell type. The antibody permitted chymase-containing mast cells to be detected in formalin-fixed tissues, and the numbers identified were similar to those in tissues fixed with Carnoy's or ethanol fixatives. Immunocytochemistry with antibody CC1 provides for the first time a sensitive and specific means for the detection of chymase in routinely fixed tissues and should prove valuable in studying mast cell subsets in disease.
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PMID:The detection of mast cell subpopulations in formalin-fixed human tissues using a new monoclonal antibody specific for chymase. 1045

Endogenous prostaglandin E2 has been indicated to have an important role in preventing gastric mucosal damage from noxious agents (i.e., in adaptive cytoprotection). However, the response of endogenous prostaglandin E2 to a mild irritant is controversial. In this study, we attempted to determine whether pretreatment with a low concentration of ethanol could induce endogenous prostaglandin E2 production by isolated canine fundic mucosal cells and to identify cells that are responsible for an increase of prostaglandin E2 production. Canine fundic mucosa was digested by collagenase, dispase, and EDTA. The cells were separated into five fractions with an elutriator rotor. Pretreatment with 5% ethanol induced a significant increase of prostagladin E2 release only from the secondary small-sized cell fraction, which was rich in mast cells and endocrine cells, and not from the other four fractions. Further cell separation by density gradient centrifugation revealed that the mast cell-enriched fraction (54%) was responsible for the increase of prostaglandin E2 release induced by the pretreatment with 5% ethanol. The results suggest that mast cells of the gastric mucosa play an important role in the production of endogenous prostaglandin E2 in adaptive cytoprotection.
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PMID:Pretreatment with mild irritant enhances prostaglandin E2 release from isolated canine gastric mucosal mast cells. 1048 24

Barium ions precipitate inorganic as well as organic sulfate compounds and they can be detected by a reaction with sodium rhodizonate. In this work, we describe the use of a barium method for the selective demonstration of sulfated glycosaminoglycans in cytoplasmic granules of mast cells and basophilic leukocytes. Methanol-fixed smears of mouse peritoneal mast cells and rat bone marrow basophils were treated with 5% BaCl2 for 10 min, followed by staining with either 0.2% sodium rhodizonate in 50% ethanol for 2 h at 60 degrees C, or 0.01% brilliant green in distilled water for 1 min. Light microscopic observation revealed a strong staining reaction of the cytoplasmic granules of these cell types, which was more selective when using sodium rhodizonate. Control smears treated with BaCl2 or sodium rhodizonate alone, and those subjected to methylation/extraction of sulfate groups before staining remained unstained. The selective binding of barium ions to mast cell granules was established with scanning electron microscopy using a backscattered electron detector, and confirmed by energy dispersive X-ray microanalysis as well as element mapping.
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PMID:A barium method for the cytochemical detection of sulfated glycosaminoglycans in mast cells and basophilic leukocytes. 1061 28


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