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)

Mast cells are unique tissue cells with high affinity surface receptors for IgE and the capacity to synthesize and store histamine in mediator-containing cytoplasmic granules that stain metachromatically upon exposure to cationic dyes. The prominence of mast cells in the gastrointestinal tract and the potential effects of newly generated and preformed mediators released by stimulated mast cells on surrounding gastrointestinal tissues have raised important questions regarding the role of the mast cell in both physiologic and pathophysiologic events in the gut. The elucidation of the role of the mast cell in the gastrointestinal tract is a complex task as illustrated by studies revealing the presence of heterogeneous populations of mast cells in this organ. Morphologic, biochemical, and functional differences have been demonstrated between mast cells located primarily in the mucosa (atypical or mucosal mast cells) and mast cells distributed throughout the connective tissues of the gut (typical or connective tissue mast cells). Awareness of the distinguishing features of mast cell populations in the gut is an important step in unraveling the functional role of gastrointestinal mast cells and may lead to the development of innovative therapeutic approaches to gastrointestinal diseases in which mast cell activation occurs.
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PMID:Intestinal mucosal mast cells. 331 86

Intestinal anaphylaxis is associated with disturbances in gut function that are antigen-specific and dependent on mast cell degranulation. Using an animal model of intestinal anaphylaxis, we have correlated alterations in water and electrolyte transport, associated with intraluminal challenge, with specific intestinal mucosal mast cell degranulation by following systemic as well as local release of rat mast cell protease II. This protease is specific for intestinal mucosal mast cells and is known to selectively attack type IV collagen, which is found in basement membranes. Intraluminal antigen challenge in sensitized animals dramatically increased serum and intraluminal levels of rat mast cell protease II. Serum levels continued to rise throughout the duration of antigen challenge. Although light microscopy of challenged intestine demonstrated little distortion of mucosal architecture, ultrastructural examination revealed significant disruption to the basement membrane and underlying collagenous matrix of the intestinal mucosa. Our findings indicate that during mucosal immunoglobulin E-mediated reactions, rat mast cell protease II is released and is associated with ultrastructural changes in the intestinal mucosa. The systemic appearance of this specific protease provides a serum marker of intestinal anaphylaxis.
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PMID:Mast cell protease release and mucosal ultrastructure during intestinal anaphylaxis in the rat. 342 67

Immunization of rats with purified rat IgE myeloma (IR2) induces an IgG class autoantibody directed specifically against the IgE isotype. This has variable stimulatory effects on the serum IgE concentration in high IgE-producing BN rats but significantly decreases the serum IgE concentration in the conventional PVG.RT1u strain. We have examined the effects of inducing such an auto-anti-epsilon response on mast cell populations, as defined by their staining characteristics in BN rats. A persistent anti-epsilon response changed the proportions of mast cell types. Those containing highly sulfated, Safranin-positive granules which equate with cells described as connective tissue mast cells (CTMC) were reduced in number in skin, tongue and bone marrow, whereas the less highly sulfated, Alcian Blue-positive mast cells were increased in number in these tissues as well as in the gut, a site rich in the so-called mucosal mast cell. The overall number of mast cells in nonmucosal sites was not significantly changed in anti-IgE-producing rats. The direct effects of anti-epsilon antiserum on mast cells in vivo were investigated using an immediate skin response (ISR) technique. The IgG component of serum from IR2-immunized rats, fractionated by high performance liquid chromatography or eluted from Sepharose 4B-coupled IR2, gave positive ISR in naive rats. The ISR was inhibited by prior incubation of immuno-purified rat anti-IR2 with solid-phase IR2 or with two unrelated IgE myeloma proteins but not with rat IgG. Histological examination confirmed that degranulation of CTMC had occurred at the ISR sites.
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PMID:Induction of an auto-anti-IgE response in rats. II. Effects on mast cell populations. 349 16

The mucosal and connective-tissue mast cells (MMC and CTMC, respectively) of the rat are histochemically and functionally distinct. MMC, unlike CTMC, are insensitive to the degranulating action of the mast cell secretagogue Compound 48/80 and instead increase in number after treatment with this drug. T cell-derived growth factors are necessary for the growth of MMC-like cells from hemopoietic tissues in vitro, as well as for nematode-induced MMC proliferation in vivo. We therefore examined the possible role of the thymus in the pharmacologically induced MMC expansion. Mast cell numbers and histamine content after treatment with Compound 48/80 were determined in the skin, tongue and gut of athymic male LEW/MOL-rnu/rnu rats and their normal littermates at the age of 6-7 weeks. The influence of the strain of rat and the mode of administration of the drug was assessed by studying age- and sex-matched Sprague-Dawley rats as well. Injections of Compound 48/80 for 5 days resulted in a statistically significant increase in the number of intestinal MMC and the histamine content of all thymus-bearing rats. The increase was more pronounced in the Sprague-Dawley rats, however, and unrelated to the mode of administration of the drug, indicating that the MMC-stimulating action of Compound 48/80 is at least partly controlled by genetic factors. Athymic rats showed no statistically significant MMC expansion. This suggests that the MMC response after Compound 48/80 treatment may be at least partly dependent on the thymus. The mast cell numbers and histamine content in the tissues of athymic control rats were higher than in their thymus-bearing littermates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thymus dependence of compound 48/80-induced mucosal mast cell proliferation. 349 96

The involvement of serotonin in the regulation of intestinal mastocytopoiesis and inflammation has been investigated in mice infected with Trichinella spiralis. Two serotonin antagonists, methysergide and ketanserin, were examined for their ability to interfere with jejunal pathology comprising the influx of mucosal mast cells and other inflammatory cells during an infection with T. spiralis and with worm expulsion. In vitro analysis of the frequency of mast cell precursors in bone marrow, blood, spleen and intestinal tissue suggested that the mucosal mast cell response during a T. spiralis infection is probably due to invasion and local maturation in the gut of mast cell precursors, and may be mediated by T-cell-derived mast cell growth factors. Since both serotonin antagonists inhibited the mucosal mast cell response in T. spiralis-infected mice and diminished the influx of eosinophilic granulocytes, goblet cell hyperplasia, and villous atrophy, it was concluded that during a T. spiralis infection in mice release of serotonin may provide an environment that facilitates the local influx in the gut of inflammatory cells. Since worm expulsion was not affected by the serotonin antagonists, these results suggest that worm expulsion can occur without a mast cell and or eosinophilic granulocyte influx. The role of serotonin release by as yet unidentified serotonin-containing cells in the gut in relation with T cell regulation is discussed.
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PMID:Involvement of serotonin in intestinal mastocytopoiesis and inflammation during a Trichinella spiralis infection in mice. 357 May 25

The frequency of precursor cells capable of giving rise to cells with characteristics of mucosal mast cells in tissues from thymus-bearing and non-thymus-bearing (nude) mice orally infected with Trichinella spiralis was determined with an in vitro assay. Analysis of the frequency of mast cell precursors in bone marrow, blood, spleen and small intestinal tissue revealed similar frequencies of mast cell precursors in bone marrow from both thymus-bearing and athymic mice. These frequencies in bone marrow were not affected by infection. However, in blood and spleen from thymus-bearing mice at Day 7 post-infection (p.i.), and in the gut at Day 14 p.i., significant increases of mast cell precursor frequencies were detected. In contrast, no significant increase was observed in the tissues of infected nude mice. These data are in accordance with in vivo findings, indicating that a mucosal mast cell response in the gut is both thymus and antigen dependent. It was concluded that a mucosal mast cell response to infection with T. spiralis is probably due to local proliferation and maturation of residing mast cell precursors, that this response might be amplified by an influx of precursor cells from the blood into the gut, and that both phenomena are T-cell dependent.
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PMID:Effect of a Trichinella spiralis infection on the distribution of mast cell precursors in tissues of thymus-bearing and non-thymus-bearing (nude) mice determined by an in vitro assay. 358 12

Coeliac disease is a malabsorptive disorder caused by intolerance to gluten and is characterized by a remodelling of the intestinal mucosa including villus atrophy, crypt hyperplasia and net increase of mucosal volume. Changes of the number of mucosal mast cells (MMCs) in coeliac mucosa has recently been reported, suggesting that the mast cell activity could have a pathogenetic role in gluten enteropathy. MMCs located solely in the lamina propria are the main repository for small-gut mucosal histamine. A consecutive prospective study was designed to study the histamine content, MMC numbers, and the relative volume of lamina propria in intestinal biopsies from adult patients suffering from unexplained diarrhea and/or malnutrition. Histamine was measured by a HPLC-method, the number of MMC was counted after long toluidine-blue staining, and the relative volumes of lamina propria and epithelium were estimated morphometrically. The findings were correlated to the histopathological appearance of the mucosa. As compared to controls the histamine content increased by 80% and MMC numbers by about 60% in the coeliac mucosa. There was also a correlation between MMC numbers and histamine content for both normal and coeliac mucosae (r = 0.81). The morphometric estimation of the relative volumes of epithelium and lamina propria revealed that the lamina-propria compartment was increased by approximately 40% in coeliac mucosa. Taking the changes in compartmental volumes of the remodelled coeliac mucosa into account, our results suggest that the histamine content and MMC population were significantly increased. MMC and MMC-associated histamine may therefore be involved in the pathogenesis of gluten enteropathy.
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PMID:Histamine and mucosal mast cells in gluten enteropathy. 372 11

Previous studies have established that the gut nematode Trichinella spiralis induces a dramatic thymus dependent intestinal mastocytosis which peaks within 6 to 12 days after primary oral infection. It is not known, however, if the increase in gut mast cells results from the influx of mast cells or their precursors, or from the expansion and differentiation of mast cell precursors (MCP) that are normally present in the small intestinal epithelium. In the present study, the number of mucosal MCP in the intraepithelial lymphocyte (IEL) population and in bone marrow (BM) cells from normal and 4 day T. spiralis infected mice was compared by culturing the cells at limiting dilutions in medium containing interleukin-3 (IL-3). While the MCP frequency in IEL from infected mice was found to be significantly increased in comparison with that found in normal mice, the numbers of MCP in BM from the two groups were equivalent. Resident intraepithelial mucosal MCP therefore undergo a local expansion before the occurrence of an overt T dependent intestinal mastocytosis. This finding lends support to the view that local mucosal T cells are involved in regulating mast cell numbers in response to intestinal helminth infection.
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PMID:Limit dilution analysis of mast cell precursor frequency in the gut epithelium of normal and Trichinella spiralis infected mice. 377 78

Changing numbers of mast cells were observed in precancerous and cancerous lesions of the gut in mice treated by 1, 2-dimethylhydrazine dihydrochloride. The study included 18 samples of abnormal and atypical epithelium, 14 samples of preinvasive carcinoma, 15 samples of infiltrative carcinoma, and 12 control samples from untreated mice. Carcinogenesis was accompanied by a significant increase of mast cell numbers culminating in preinvasive carcinoma. A decrease of mast cells followed in fully developed adenocarcinomas up to numbers comparable to but more variable than those found in abnormal and atypical epithelium.
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PMID:[Mastocytes in the process of cancerogenesis. I. Study of experimental model systems]. 379 52

Rats primed by infection with the intestinal nematode Nippostrongylus brasiliensis and challenged intravenously with soluble whole-worm antigen undergo systemic anaphylactic shock. The primary lesions are in the gut and include increased permeability of the mucosa together with release, into enteric secretions, of a mucosal mast cell (MMC)-specific serine proteinase, rat mast cell protease II (RMCP-II). This enzyme is also released into the blood of shocked rats. These manifestations of anaphylaxis were abolished in rats previously treated with corticosteroids (methylprednisolone acetate, 25 mg per kg of body weight, 48 and 24 hr before i.v. challenge with antigen). Suppression of the response was associated with depletion of RMCP-II and of MMC from the intestinal mucosa. Depletion occurred 4-24 hr after treatment with as little as 1 mg of methylprednisolone per kg. By contrast, neither connective tissue mast cells nor serum levels of parasite-specific IgE were depleted in rats given 2 X 25 mg of methylprednisolone per kg. The capacity of unprimed treated rats to mount passive cutaneous anaphylaxis was, however, impaired.
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PMID:Depletion of mucosal mast cell protease by corticosteroids: effect on intestinal anaphylaxis in the rat. 388 54


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