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)

Differential nasal responsiveness to environmental tobacco smoke (ETS) has been documented in humans and we hypothesized that this reflects differential responsiveness to c-fiber stimulation. We compared the response to intranasal capsaicin in subjects with and without a history of ETS-rhinitis. We challenged 10 ETS-sensitive and 11 ETS-nonsensitive subjects intranasally with 25 mg of lactose powder followed by 25 pg to 25 ng of capsaicin in 25 mg of lactose. Subjects rated nasal symptoms and underwent nasal lavage. In each lavage, the concentrations of albumin (an index of vascular permeability), kinins and histamine (a marker of mast cell activation) were measured. Nasal lavage tosyl-L-arginine methyl ester (TAME)-esterase activity, which can be a reflection of mast cell activation, increased vascular permeability or glandular secretion, was also determined. Subjects with a history of ETS-rhinitis reported more rhinorrhea than subjects without a history of ETS-rhinitis (P less than .01). No significant increase occurred in nasal lavage histamine, albumin or kinins in either subject group. TAME-esterase activity (presumably a reflection of increased glandular secretion) increased greater than 1000 cpm in 12/21 subjects (designated "TAME-producers"), but this was unrelated to ETS-sensitivity. TAME producers showed a dose-dependent increase in TAME-esterase activity, whereas TAME nonproducers showed no change at any capsaicin dose. We conclude that capsaicin causes nasal symptoms and glandular stimulation without evidence of increased vascular permeability or mast cell activation. ETS-rhinorrhea symptoms in humans appear related to c-fiber stimulation. The absence of c-fiber-induced glandular secretion, although not related to ETS-sensitivity, was associated with decreased sneezing and increased symptoms of capsaicin-induced nasal burning.
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PMID:Effect of intranasal capsaicin on symptoms and mediator release. 176 79

Previous studies have shown that nasal allergen provocation leads to dose-dependent increases of inflammatory mediators, e.g. histamine, kinins, LTC4 and PGD2 in nasal lavages. To investigate further the interaction of these mediators, a titration study with intranasal bradykinin (Bk) application (maximal dose 100 nmol/nostril) and consecutive lavage were performed in eight grass-pollen-allergic patients out of season, and five controls. The nasal lavages were analysed for albumin, N-alpha-tosyl-L-arginine methyl ester (TAME) esterase activity, histamine, 9 alpha,11 beta-PGF2, and LTC4. The clinical reactions were measured with a subjective symptom score. A dose-dependent elevation of albumin was found which was significantly higher in patients with allergic and non-allergic rhinitis compared with normal volunteers. TAME-esterase activity also increased in relation to the dosage of Bk given without significant difference between the various groups. No influence on histamine, LTC4 and 9 alpha,11 beta-PGF2, release (PGD2 metabolite) was seen. Short-lasting clinical symptoms like irritation, sneezing, and obstruction were noticed after the two highest Bk dosages (10 and 100 nmol). We conclude that intranasally applied Bk induces a dose-dependent plasma leakage into the nasal cavity, which is significantly higher in patients with seasonal allergic rhinitis out of season compared to normals. Bk does not seem to affect the mast cell since histamine, LTC4 and 9 alpha,11 beta-PGF2 levels do not alter. The ability to induce relevant symptoms of rhinitis provides strong support for the hypothesis that kinins may be important mediators of inflammatory disorders of the upper airways.
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PMID:Nasal challenge studies with bradykinin: influence upon mediator generation. 191 65

The number of mast cells in the inferior turbinate from patients with perennial allergy due to house dust mite were compared with ten normal controls. Ten random high powered fields were counted in the epithelium and the submucosa in samples which had been divided into two and fixed either in aqueous formalin or Carnoy's fixative. The sections from each block were stained with either Azure A or Chloroacetate esterase technique. No statistical differences were found. The lack of increase in mast cell numbers was attributed to degranulation since numbers have been shown to be increased in perennial allergy when sections are examined ultrastructurally.
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PMID:Mast cell numbers in the mucosa of the inferior turbinate in patients with perennial allergic rhinitis: a light microscopic study. 191 42

Three cases of splenic involvement in three different types of generalized mastocytosis (systemic mast cell disease) are reported. The macroscopic, histological and ultrastructural modifications of the spleen are described. Each case exhibited a different morphological pattern. Giemsa staining, fluorescence after acridine orange staining and naphthol ASD chloracetate esterase reaction are shown to be valuable for diagnosis. By comparison, immunohistochemistry seemed not to be very useful, because no specific antigens are expressed. These findings are compared to previously published cases. Their value for the diagnosis and the prognosis are discussed.
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PMID:Different patterns of spleen involvement in systemic and malignant mastocytosis. A histological and immunohistochemical study of three cases. 194 10

The activation of mast cells is generally considered to be an important trigger mechanism in the immediate allergic response. This study focused on the determination of three markers of mast cell activation after an allergen challenge. Nasal allergen challenges were performed in 25 subjects with seasonal allergic rhinitis using three allergen doses increasing in 10-fold steps in a standardised nasal lavage model for the subsequent recovery of the markers of mast cell activation. The levels of histamine and tryptase in the nasal lavage fluid were determined using radioimmunoassays, while the TAME-esterase activity was determined using a radiochemical technique. The nasal symptoms obtained on challenge were assessed using a scoring technique. The allergen challenge resulted in significant increases in the levels of all three markers, tryptase, histamine and TAME-esterase. In the individual measurements after the challenges there was a highly significant correlation between the TAME-esterase levels and the tryptase levels (r = 0.71; P less than 0.001), while the generation of histamine and tryptase was not significantly correlated. When comparing the cumulative generation of the three markers, significant correlations were found between all three. Allergen challenges in six non-allergic controls using the same technique did not result in any increase in tryptase levels. The findings suggest that the determination of tryptase in nasal lavage fluid may be a valuable indicator of mast cell activation in the upper airways.
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PMID:Tryptase in nasal lavage fluid after local allergen challenge. Relationship to histamine levels and TAME-esterase activity. 195 95

We describe a patient with fever and multiple osteolytic bone lesions accompanied by hypercalcemia, a duodenal ulcer, anemia, and thrombocytopenia. Bone marrow showed a dense infiltration by abnormal cells characterized by small basophil granula, erythrophagocytosis and nuclear atypia. These cells were positive for toluidine blue and partly for myeloperoxidase and chloroacetate esterase, expressed myeloid differentiation markers, and exhibited multiple numerical and structural chromosome aberrations. Molecular genetic analysis showed no breakpoint cluster region rearrangement. Electron microscopy demonstrated granula both of basophil and mast cell type. Concluding, in this patient an acute hematopoietic malignancy with many features of malignant mastocytosis but also with signs of a basophil differentiation. This is further support for a hematopoietic stem cell origin of human mast cells.
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PMID:Philadelphia chromosome-negative acute hematopoietic malignancy: ultrastructural, cytochemical and immunocytochemical evidence of mast cell and basophil differentiation. 210 68

The effects of sulfonates on the carboxypeptidase A catalyzed hydrolysis of the ester substrate benzoylglycyl-L-phenyllactate were determined. The modifiers examined were benzenesulfonate, p-toluenesulfonate, 2-phenylethane-sulfonate, methanesulfonate, ethanesulfonate, propanesulfonate, butanesulfonate, pentanesulfonate, hexanesulfonate, heptanesulfonate, and 2,2-dimethyl-2-silapentane-5-sulfonate. Sulfonate activators of peptide hydrolysis were inhibitors of esterase activity. Of the sulfonates studied, 2,2-dimethyl-2-silapentane-5-sulfonate was the most effective inhibitor. 2-Phenylethanesulfonate, hexanesulfonate, heptanesulfonate, and 2,2-dimethyl-2-silapentane-5-sulfonate exhibited uncompetitive inhibition. The remaining sulfonates either did not inhibit or the inhibition was too weak to properly characterize.
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PMID:Effect of sulfonates on the esterase activity of carboxypeptidase A. 222 15

The number of DNA synthesizing mast cells in experimental induced wounds was calculated using bromodeoxyuridine as a DNA marker and naphthol AS-D chloroacetate esterase as a mast cell marker. After different survival times, specimens of the wound edge were taken before death and 24 hs after death. At a survival time of 48 hs in vital biopsy the number of DNA synthesizing mast cells peaked, at 72 hs and fell after a period of 8 days. Even though an identical kinetic course was demonstrable in cases of postmortal biopsies the percentage at each survival period was significantly lower than in vital biopsies.
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PMID:[Quantitative studies of mast cell proliferation at the wound edge --rate of DNA synthesis in intravital and postmortem biopsy]. 224 3

Exogenous addition of purified chymase, a rat serosal mast cell (RSMC) chymotryptic enzyme, results in RSMC degranulation at 37 degrees, but not at 1 degree. Chymase can cause an active site-dependent inducing event at 1 degree such that RSMC degranulation occurs if the cells are later incubated at 37 degrees. RSMC exposed to chymase or other stimuli were surface radiolabelled using 125I and Iodo-Gen, solubilized with 1% Nonidet-40, and the resulting 25,000 g supernatants analysed by SDS-PAGE and autoradiography. A 125I-labelled RSMC membrane protein of approximate 90,000 MW decreased upon exposure to either chymase or alpha-chymotrypsin (alpha-CT) for 5 min at 37 degrees or to chymase for 60 min at 1 degree. Exposure of RSMC to the secretagogues ionophore A23187, compound 48/80, and anti-IgE for 5 min at 37 degrees resulted in beta-hexosaminidase (a secretory granule enzyme) release, but did not cause a detectable change in the 90,000 MW surface-labelled protein. Lima bean trypsin inhibitor, which inhibits both the esterase and RSMC degranulation activities of chymase and alpha-CT, prevented the disappearance of the 125I-labelled 90,000 MW band when added with chymase or alpha-CT. Exposure of RSMC to chymase at 1 degree for 0-10 min, prior to addition of LBTI, led to a progressive disappearance of the 90,000 MW band, which corresponded to the kinetics of priming for subsequent RSMC degranulation at 37 degrees. When RSMC were exposed to trypsin (2.5 micrograms/ml) for 0-120 min at 1 degree, a progressive disappearance of the 90,000 MW band occurred, in association with a loss of sensitivity to subsequent activation by chymase at 37 degrees. The disappearance of the 90,000 MW determinant in association with chymase-mediated priming for degranulation and the inability of chymase to mediate degranulation of trypsin-treated RSMC, which lack this membrane protein, suggests that it is involved in chymase-mediated RSMC degranulation.
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PMID:Cleavage of a rat serosal mast cell membrane component during degranulation mediated by chymase, a secretory granule protease. 231 65

Several studies have indicated that mast cells occur in close proximity to enteric nerves in the gastrointestinal tract of rats, man, and other mammalian species, and such intimate associations have been proposed as one of the anatomical bases of communication between the immune and the nervous systems. However, the specificity of anatomical associations between enteric nerves and mast cells, as opposed to other bone marrow-derived or lymphoid cells normally present in mucosal sites, is unclear. We used transmission electron microscopy to quantify the distances between mast cells and neural processes (nerve terminals or axons) in the small intestinal mucosa, right atrium, skin, and pulmonary parenchyma of normal rats, and in the small intestinal mucosa and lung parenchyma of rats that had undergone hyperplasia of the mast cell populations in these sites as a result of infection with the nematode Nippostrongylus brasiliensis. In the jejunal mucosa of normal rats, 8.0% of mast cells occurred within 100 nm of neural processes and an additional 11.0% between 101 and 500 nm of these structures; the corresponding figures for eosinophils were 3.3% (N.S. vs. mast cell value) and 23.3% (p less than 0.05 vs. mast cell value) and for plasma cells were 8.5% and 14.6% (N.S. vs. mast cell values). In the right atrium, 1.2% of mast cells occurred within 100 nm and an additional 13.4% within 101 and 500 nm of neural processes, whereas no mast cells were observed within 500 nm of neural processes in the pulmonary parenchyma or ear skin. Infection with N. brasiliensis increased by 61% the proportion of mast cells within 500 nm of neural processes in the jejunal mucosa and resulted in the appearance of mast cells in close association with these structures in the jejunal muscularis propria, but had no effect on the proportion of mast cells within 100 or 500 nm of neural processes in the pulmonary parenchyma. Acetylcholine esterase staining demonstrated dense networks of neural processes in the three sites where some mast cells were closely associated with these structures (jejunal mucosa and muscularis, right atrium) but not in the pulmonary parenchyma or ear skin. Taken together, our findings indicate that mast cells occur in close proximity to neural processes in sites where these structures are abundant, but that anatomical associations as close as those between mast cells and neural processes can also occur between such structures and other bone marrow-derived cells (eosinophils) or lymphoid cells (plasma cells) resident in the small intestinal mucosa.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Anatomical variation in mast cell nerve associations in the rat small intestine, heart, lung, and skin. Similarities of distances between neural processes and mast cells, eosinophils, or plasma cells in the jejunal lamina propria. 234 32


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