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)

Endoscopic gastrointestinal mucosal biopsy specimens from one patient with systemic mastocytosis and five with urticaria pigmentosa (UP) were fixed with Carnoy's reagent and then stained for chloracetate esterase. The mast cell population densities were enumerated in the mucosa using cursor planimetry. Compared with controls, mast cell counts were increased in gastric and duodenal but not sigmoid mucosae. On a histological basis, systemic involvement would appear commoner in urticaria pigmentosa than is generally expected. Gastrointestinal symptoms did not relate to elevated mucosal mast cell counts.
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PMID:Intestinal mucosal mast cells: enumeration in urticaria pigmentosa and systemic mastocytosis. 320 11

Kinins are generated in nasal secretions during allergic reactions and during induced rhinovirus colds. To determine if kinins may contribute to the symptomatology of these inflammatory reactions, 8 subjects were challenged with increasing doses of bradykinin or with placebo. Levels of albumin, histamine, and N-alpha-tosyl-L-arginine methyl ester (TAME)-esterase were measured in nasal lavages, and symptom scores were noted. No symptoms or increases in mediators or protein were observed after placebo challenge. Symptom scores increased in a dose-dependent manner, however, in response to bradykinin challenge. Increased symptoms were associated with significant increases in albumin and TAME-esterase activity, but no increases in histamine were observed. Nasal conductance measurements confirmed that bradykinin induces dose-dependent unilateral obstruction in the challenged nostril. Other common symptoms were rhinorrhea and, of particular relevance to rhinovirus infections, a persistent sore throat. We conclude that bradykinin causes increased vascular permeability and rhinitis, which are independent of mast cell mediator release. Kinins may, therefore, contribute to the symptomatology of inflammatory reactions of the upper airways, including the common cold.
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PMID:Nasal provocation with bradykinin induces symptoms of rhinitis and a sore throat. 334 41

To investigate the pathogenesis of allergic rhinitis, we developed a nasal challenge model in which we examined the early, late, and rechallenge responses to antigen provocation. In these three aspects of the allergic reaction the physiologic responses are associated with inflammatory mediator release. Whereas the early response appears to be related mainly to mast cell activation and mediator release, the late reaction involves a different pattern of mediator release and an inflammatory cell influx, consisting of basophils, neutrophils, and eosinophils. Rechallenge with antigen 11 hours later results in an augmented immediate response. Pretreatment with aspirin reduces the levels of cyclooxygenase metabolites in nasal secretions without affecting the immediate physiologic response to antigen or the expected increase in the levels of histamine, N-alpha-tosyl-L-arginine methyl ester-esterase activity, and leukotriene C4. Pretreatment with systemic steroids does not affect the early allergic response, but significantly reduces mediator release during the late and rechallenge responses. The influx of eosinophils is inhibited by pretreatment with systemic steroids, but neutrophil influx is not. In contrast, pretreatment with topical steroids blocks the early response and the late and rechallenge responses. Influx of all cell types, including the neutrophil, was prevented. These studies show unequivocally that an inflammatory process follows the initial response to antigen and that this inflammation is affected by drugs important in the treatment of chronic allergic disease. We speculate that understanding allergic inflammation will lead to new therapeutic development.
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PMID:Experimentally induced nasal allergic responses. 337 15

Globule leukocytes in the epithelium of the rat trachea may be counterparts of mucosal mast cells that are located in the gastrointestinal tract. If they are indeed similar to mucosal mast cells, globule leukocytes would be expected to decrease in number in rats treated with dexamethasone but not in rats treated with compound 48/80, an agent which causes non-antigenic degranulation of connective tissue mast cells. In this study, we determined the number and compared the distribution of globule leukocytes and connective tissue mast cells in the tracheas of pathogen-free rats. We then determined whether the number of these two types of cells changes in rats treated for 5 days with compound 48/80, dexamethasone, a combination of compound 48/80 and dexamethasone, or saline. We identified globule leukocytes and mast cells in whole mounts and histological sections of rat tracheas by using a histochemical reaction that demonstrates the chymotrypsin-like protease (chloroacetate esterase) present in mast cell granules. Using this method, we found that approximately 225,000 globule leukocytes were present in the epithelium of the trachea. These cells were most abundant in the rostral trachea. Rats treated with dexamethasone had a 91% reduction in the number of globule leukocytes with protease-containing granules, but rats treated with compound 48/80 had a normal number of these cells. We found some 55,000 connective tissue mast cells in the same tracheas. Mast cells were most abundant in the posterior membrane of the caudal trachea and in the lamina propria between cartilaginous rings. Rats treated with compound 48/80 had a 96% reduction in mast cells with protease-containing granules, but rats treated with dexamethasone had a normal complement of mast cells. We conclude that globule leukocytes are abundant in the tracheas of healthy rats, are similar in morphology and pharmacological responses to mucosal mast cells located in other organs of rats, and are more numerous than and have a different distribution than connective tissue mast cells. Globule leukocytes in the tracheal epithelium may have a role in respiratory defenses similar to that of mucosal mast cells in other organs.
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PMID:Globule leukocytes and mast cells in the rat trachea: their number, distribution, and response to compound 48/80 and dexamethasone. 339 53

A variety of modifiers of carboxypeptidase A (CPA) have been investigated in an effort to understand the structural requirements of inhibitors and activators of peptidase activity. It is proposed that an understanding of the mechanism of action of reversible activators of the enzyme may bear on the long standing question of whether the detailed mechanism of peptidase activity is different from that of esterase activity. An analog of the activator 2,2-dimethyl-2-silapentane-5-sulfonate, 5,5-dimethylhexanoate, was found to be a competitive inhibitor of the CPA-catalyzed hydrolysis of benzoylglycyl-L-phenylalanine. The modifier 4-phenyl-3-butenoate (styrylacetic acid) was determined to be an activator. The sulfonates benzene-sulfonate, p-toluenesulfonate, phenylmethanesulfonate, 2-phenylethanesulfonate, and 3-phenylpropanesulfonate were all found to be activators.
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PMID:Kinetic studies of modifier effects on the carboxypeptidase A catalyzed hydrolyses of peptides. 343 67

Primary cultures of adherent rheumatoid synovial cells contain variable proportions of fibroblasts, macrophages, and dendritic cells, as judged by morphological appearance. Comparative studies using various enzymic and histochemical staining procedures showed the dendritic cells to lack many of the characteristic features of macrophages, e.g. the failure to express HLA-DR (Ia) antigen. The dendritic cells and fibroblasts had several similarities, but differed to some extent in their nonspecific esterase activity, phagocytic and proliferative potential. As the proportions of dendritic cells and fibroblasts varied in relation to specific culture conditions, we examined the possibility that these morphologies might represent different functional states rather than distinct cellular origins. Using subcultured synovial fibroblasts with a uniform bipolar appearance, we have shown that exposure to interleukin-1 or mast cell products resulted in a transformation to dendritic morphology. This change in cell shape was prevented by the presence of indomethacin, but was subsequently achieved by the addition of exogenous PGE2. Thus it appears that the latter is the factor that modulates the morphological change of fibroblastic to dendritic cells. This study has also demonstrated the complete and reversible interchange of fibroblast/dendritic morphology, thereby confirming that these different shapes are manifest by the same cell. The changes in phenotypic expression associated with the dendritic appearance include increased production of collagenase, prostaglandin E, and nonspecific esterase, as well as an apparent inability to exhibit phagocytosis and to proliferate in culture. We conclude from our in vitro studies that the phenotypic behaviour of the synovial fibroblast (or synoviocyte) is very variable and dependent to a large extent upon local stimuli, but the identity and hierarchy of such stimulating and suppressive factors in relation to cellular interactions requires further study.
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PMID:Comparative studies of adherent rheumatoid synovial cells in primary culture: characterisation of the dendritic (stellate) cell. 349 52

A series of 70 patients with the squamous cell carcinoma of the lip and followed-up for at least 5 years, was assessed on light microscopy and using histochemical staining for ANAE (acid-naphthyl acetate esterase) to demonstrate the morphological manifestations of tumor-host reactivity. The factors analysed include cancer differentiation (intrinsic malignancy) and stromal reactions (intensity of the immunocompetent cell infiltrate including the mast cells and the subpopulations, i.e. B- or T lymphocytes or mononuclear phagocytes). Differentiation of the lip cancer was shown to be directly (although not statistically significantly) related to the 5-year survival, as was also the intensity of the stromal immunocompetent cell infiltration. Cancer metastases were evidently the most powerful prognostic determinants, their development being influenced both by the intensity of the stromal immunocompetent cell infiltrate and cancer differentiation. B lymphocytes far outnumbered the T and MPS cells in all the infiltrates studied, the percentages of the latter two cell types, however, being inversely related to the intensity of the infiltrate. The cell composition in the infiltrates was seemingly without effect on the frequency of metastases and the 5-year survival, as was the stromal mast cell reaction, too. It was concluded that analysis of tumor-host relationships using a variety of morphological and immunohistochemical techniques may be of benefit in predicting the clinical course of lip cancer.
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PMID:Tumor differentiation and tumor-host interactions as prognostic determinants in squamous cell carcinoma of the lip. 351 41

The catalytic properties of a sheep mast cell proteinase (SMCP), isolated from abomasal mucosal mast cells, were investigated. The enzyme was shown to have chymotrypsin-like esterase activity, with no detectable amide activity, using a range of low molecular weight substrates. Maximal activity, against Benzyloxycarbonyl-L-tyrosine-4-nitrophenol ester, was determined to be in the range pH 7.6-8.0. Inhibitor studies showed that, unlike chymotrypsin, a serine proteinase, SMCP was found to be susceptible to the action of thiol blocking agents and chelating agents, but to be unaffected by diisopropylphosphofluoridate, a serine proteinase inhibitor.
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PMID:The catalytic properties of a proteinase isolated from sheep abomasal mucosal mast cells. 353 58

An autopsy case of systemic mastocytosis without cutaneous involvement in a 76-year-old woman was described. The patient presented with general malaise, chest and epigastric discomfort, flushing of the face and progressive hepatosplenomegaly, and she terminated in hemorrhagic complications of DIC within 2 months. There was neither rash nor urticaria pigmentosa recognizable in the entire course. The diagnosis was made by the histologic identification of abnormal aggregates of mast cells in a bone marrow aspirate. These mast cell granules were chloroacetate esterase-positive, peroxidase-negative, and electronmicroscopically they were composed of fine granular materials containing variable numbers of lamellar structures. At autopsy, diffuse infiltration of the mast cells was found in the liver, spleen, bone marrow, lymph nodes, lungs, kidneys, stomach, and adrenal glands.
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PMID:Systemic mastocytosis without cutaneous involvement. 355 89

An intimate interplay between the host factors and the tumour seems to be operative in lip cancer, and is undoubtedly capable of modifying the clinical course of the disease. A series of 70 patients with squamous cell carcinoma of the lip was assessed by light microscopy and using histochemical staining for acid alpha-naphthyl acetate esterase to demonstrate the morphological manifestations of tumour-host reactivity. The factors analysed include stromal reactions; intensity of the immunocompetent cell infiltrate including mast cells, and the subpopulations, i.e. B or T lymphocytes and mononuclear phagocytes (MPS cells). B lymphocytes far outnumbered the T and MPS cells in all the infiltrates studied, the percentages of the latter two cell types being inversely related to the intensity of the infiltrate, however. The cell composition in the infiltrates lacked statistically demonstrable effect on the frequency of metastases and the 5-year survival, as did the stromal mast cell reaction, too.
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PMID:Immunocompetent cell reaction in prognostic evaluation of squamous cell carcinoma of the lip. 361 94


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