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)

Thirteen patients with systemic mast cell disease were studied in order to define the hepatic changes in this disease and to correlate the histologic lesions in the liver with the clinical findings. These patients often presented with multisystem disorders and 10 had hepatomegaly. Microscopically, the liver tissues in all patients showed fibrosis and chronic inflammatory cellular infiltration with plasma cells, lymphocytes, eosinophils, and mononuclear fibroblast-like cells in the portal area. The hepatic sinusoids were not significantly involved. A histologic diagnosis of systemic mast cell disease is seldom entertained in liver biopsy specimens embedded in paraffin and stained with hematoxylineosin, but can be facilitated in biopsy specimens embedded in plastic such as methacrylate. Tissue mast cells in the cellular infiltrate can be demonstrated best by special staining techniques with Giemsa, toluidine blue, and chloroacetate esterase. The severity of the histologic changes in the liver does not correlate well with the size of the liver or biochemical changes in the blood. Abnormal serum biochemical values were noted primarily in those with dehydration caused by diarrhea and vomiting, and in those with malnutrition. Hepatic function test results were usually normal, except for alkaline phosphatase level, which was elevated in all 13 patients. Although the clinical significance of hepatic involvement in systemic mast cell disease cannot be established with certainty in this study, it is believed that the prognosis of systemic mast cell disease is most intricately related to the systemic effects of mast cell involvement in many other organs, and not to hepatic involvement per se.
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PMID:Hepatic involvement in systemic mast cell disease. 370 70

We have demonstrated that kinins are generated following nasal challenge with allergen of allergic (5.6 +/- 0.17 ng/m-), but not nonallergic (0.04 +/- .02 ng/ml), individuals (n = 8 in each case). The presence of kinin was highly correlated with that of histamine and TAME-esterase activity and with clinical symptoms (p less than 0.001). In a double blind, placebo-controlled study, topical administration of the drug Azatadine, which inhibits mast cell mediator release in vitro, reduced the clinical response to allergen challenge and reduced the concentrations of kinins, histamine, and TAME-esterase activity observed following allergen challenge. In addition to the immediate response to allergen, some individuals experience a recurrence of symptoms some 3-12 hours after challenge; in seven such individuals (13.5 +/- 3.2 ng kinin/ml in the immediate reaction), there was a second increase in nasal kinins (2.95 +/- 1.4 ng/ml) during this late reaction, again correlating with increases in histamine and TAME-esterase activity. HPLC analysis revealed that a mixture of bradykinin and lysylbradykinin is produced during both responses. Finally, 12 subjects with a history of nasal symptoms upon exposure to cold, dry air (CDA) were compared to five asymptomatic individuals in a nasal challenge system involving nasal breathing of CDA and warm, moist air (WMA). For the symptomatic group the levels of kinin in nasal lavages were significantly increased after CDA (2.9 +/- 0.8 ng/ml) compared to baseline (0.06 +/- 0.01 ng/ml) or WMA (0.3 +/- 0.07 ng/ml). Kinin generation again correlated with increases in histamine, PGD2 and TAME-esterase activity and with onset of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinins as mediators of human allergic reactions. 381

A purified capillary permeability increasing-enzyme was obtained from Agkistrodon caliginosus venom by modification of our previous purification method. The purified enzyme, which had arginine esterase activity and strong capillary permeability increasing-activity, did not show caseinolytic, clotting or bradykinin-releasing activities. These properties of the enzyme were almost the same as those of the enzyme obtained by the previous purification method. When a mixture of the purified enzyme and bovine plasma or heated bovine plasma was injected into depilated skin on the back of a rabbit, the capillary permeability increasing-activity was much greater than that induced by injection of the enzyme alone. The substance which increases the capillary permeability was extracted from the incubated mixture of bovine plasma and the enzyme with 50-70% ethanol. Its activity was lost on treatment with carboxypeptidase A. From these results, it is supposed that the increase in capillary permeability induced by the enzyme is due to a low molecular weight peptide released from a protein in bovine plasma by the proteolytic action of the enzyme.
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PMID:Isolation and physiological action of capillary permeability increasing-enzyme from the venom of Agkistrodon caliginosus. 381 9

The enzyme naphthol-AS-D-chloroacetate esterase is histochemically demonstrated in the granules of globule leucocytes in the tracheal epithelium of rats. The enzyme reactivity may be used as a cytochemical marker of these cells. The previously postulated mast cell origin of globule leucocytes is doubted, and the possibility that globule leucocytes belong to the group of natural killer cells is discussed. The biological role of the located esterase and the function of the globule leucocytes are also briefly discussed.
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PMID:Naphthol-AS-D-chloroacetate esterase activity in globule leucocytes in the tracheal epithelium of rats. 395 57

Serine esterases were detected in the granules of mucosal mast cells from rat, mouse, sheep, and man. Successful demonstration of enzyme activity required brief fixation (6 h) of tissues in 4% paraformaldehyde. Staining with naphthol AS-D chloroacetate produced an intense red reaction product in intraepithelial mucosal mast cells (globule leucocytes) and mucosal mast cells within the lamina propria of the gastrointestinal tract. The mast cell identity of cells stained for esterase was confirmed by sequential staining with toluidine blue (pH 0.5). Furthermore, the numbers of cells detected after staining for esterases or with toluidine blue were highly correlated. Esterase activity within mucosal mast cells/globule leucocytes from all species was inhibited with the serine enzyme inhibitor phenylmethylsulphonyl fluoride. Further histochemical studies with the substrate, N-acetyl-DL-phenylalanine B-naphthyl ester, indicated that mucosal mast cells and globule leucocytes contain esterases which are chymotrypsin like in substrate specificity.
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PMID:Histochemical demonstration of chymotrypsin like serine esterases in mucosal mast cells in four species including man. 398 50

The pathogenesis of rhinitis was investigated using a model of nasal provocation with different types of stimuli. Allergic subjects had an immediate response to antigenic challenge with symptoms of rhinitis highly correlated with increments in the concentrations of histamine, prostaglandin D2, kinins and kininogens, leukotrienes, and toluene sulfonyl arginine methyl ester esterase activity in their nasal secretions. This reaction was abated by a tricyclic antihistamine also capable of inhibiting mediator release from human mast cells in vitro and, in some subjects, by disodium cromoglycate. In a number of patients, symptoms reappeared three to 12 hours after nasal provocation. This late reaction also involves release of all of the aforementioned mediators except for prostaglandin D2, and preliminary data suggest that it can be inhibited by oral or topical steroids. Cold, dry air can induce rhinitis with mast cell mediator release from selected subjects. The pathogenesis of this reaction is unclear, but there are indications that osmolarity changes are responsible for mast cell activation. Thus, mast cells can be induced to release mediators and cause nasal symptoms by both immunologic and physical mechanisms, which may account for the pathophysiology of several types of rhinitis.
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PMID:Mediator release during nasal provocation. A model to investigate the pathophysiology of rhinitis. 408 96

The degree of metachromasia of mast cell granules is known to vary with the type of tissue fixation and among different tissues and species. The present study sought to determine whether mast cells in dog skin are heterogeneous with respect to fixation and staining properties. We performed skin biopsies in six anesthetized, atopic dogs and one mongrel dog. One biopsy was fixed in formalin and a second, from a parallel abdominal site, was fixed in basic lead acetate (Mota's solution). Adjacent sections from each biopsy were stained with alcian blue (1%, pH 0.5) or for chloroacetate esterase activity. In alcian blue-stained sections, one-third fewer mast cells were detected in skin fixed in formalin (1,836 +/- 454 mast cells/mm3, mean +/- SEM) than in skin fixed in basic lead acetate (2,684 +/- 527 mast cells/mm3) (P less than 0.05). The chloroacetate esterase reaction detected the larger number of mast cells regardless of the fixative used. We conclude that mast cell heterogeneity, as demonstrated by metachromatic staining following different types of tissue fixation, exists in dog skin. "Typical" mast cells stain with alcian blue regardless of fixation; however, "atypical" mast cells exhibit metachromasia only after fixation in basic lead acetate. Both the typical and atypical types of mast cells have chloroacetate esterase activity.
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PMID:Mast cell heterogeneity in dog skin. 408 28

The ability of a number of p-nitrophenylethyl, alkyl phenylalkyl, chloroalkyl, and aminoalkyl phosphonates to inhibit the homocytotropic antibody-mediated release of histamine from rat peritoneal mast cells has been tested. The effectiveness of these same phosphonates against the activated first component of rat complement (C'1a) has also been investigated. The rat mast cell esterase activated by the reaction of antigen and homocytotropic antibody resembles chymotrypsin in its reactivity with the phenylalkyl and chloroalkyl phosphonate, but is unlike this protease in its greater responsiveness to the 5-aminopentyl phosphonate relative to the pentyl phosphonate. The antigen-homocytotropic antibody-activated mast cell esterase and chymotrypsin, thus, appear to be similar, but different enzymes; i.e., they are parazymes (see reference 4, p. 501). There are distinct differences in the pattern of inhibition given by the phenylalkyl and aminoalkyl and alkyl phosphonates of the homocytotropic antibody-mediated histamine release from rat peritoneal mast cells and from guinea pig lung slices. On the basis of these differences it is concluded that the esterases activated by the combination of antigen and homocytotropic antibody on the mast cells of the two species are not the same. The arithmetic dose response curve found for the action of the phosphonates on the antigen-induced histamine release from rat peritoneal mast cells contrasted sharply with the logarithmic relationship found when these same inhibitors acted on the guinea pig lung system. This suggests that in addition to the antigen-antibody-activated esterases being unlike, the detailed mode of histamine release from the mast cells of the guinea pig lung differs from that of the mast cells of the rat peritoneum. Distinct and large differences were found in the pattern of inhibition of histamine release from rat peritoneal mast cells and of rat C'1a given by the phenylalkyl, and chloroalkyl and alkyl phosphonates implying that esterase activated by the combination of antigen with the sensitized rat peritoneal mast cells is not C'1a. Thus, the results with the peritoneal mast cells lead to the same conclusion as the previous work with guinea pig lung slices; i.e., the antigen-antibody-activated esterase involved in the homocytotropic antibody-mediated release of histamine is not part of the complement system.
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PMID:Mechanisms of immunologic injury of rat peritoneal mast cells. I. The effect of phosphonate inhibitors on the homocytotropic antibody-mediated histamine release and the first component of rat complement. 416 85

There is an absolute requirement for C'1, C'2, C'4, C'3, and C'5 in releasing histamine from rat peritoneal mast cells sensitized with rabbit anti-rat gamma globulin. This conclusion is based upon the restoration of histamine-releasing capacity by adding highly purified complement components to sera deficient in one or more of these components. Of special advantage was the availability of sera from humans with inborn or acquired deficiencies in a single component. The p-nitrophenyl ethyl phosphonates block this reaction by inhibiting an antigen-antibody-activated esterase which exists in a phosphonate resistant precursor state until activated by the interaction of the sensitized mast cell and serum complement. There is almost complete disparity between the ability of the phosphonates to inhibit complement-dependent histamine release by rabbit anti-RGG and to inactivate C'1a. Even though C'1a is required for complement-dependent histamine release by rabbit anti-RGG, this is not the esterase being blocked by the phosphonates under the experimental conditions used. The pattern of inhibition by the phosphonates of the antigen-antibody-activated esterase required for complement-dependent, noncytotoxic histamine release is remarkably similar to that of the esterase required for homocytotropic antibody-mediated histamine release. One possible implication is that these two quite different modes of carrying out antigen-antibody-induced histamine release from rat peritoneal mast cells lead to activation of the same esterase and share a common pathway.
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PMID:Mechanisms of immunologic injury of rat peritoneal mast cells. II. Complement requirement and phosphonate ester inhibition of release of histamine by rabbit anti-rat gamma globulin. 416 86

To test the hypothesis that viral respiratory infections cause symptoms by activating mucosal mast cells to release mediators active on vasculature and mucosal glands, the presence of histamine in nasal secretions was assessed during natural colds and rhinovirus infections. Secretions were collected either with saline washes of the nasal cavity or by forcibly blowing into a beaker, and histamine was assayed spectrofluorometrically. In blown secretions from uninfected subjects, large variations were seen between individuals (ranging from 3 +/- 2 to 59 +/- 32 ng/ml), and equally large variations were seen from day to day in given subjects. Infection with rhinovirus and with influenza A did not change these concentrations significantly. In general, both with blown nasal secretions and with nasal washes, histamine concentrations tended to be lower during infection. Concentration of another preformed mast cell mediator, TAME-esterase, also was not elevated during infection. Thus, these data do not support an hypothesis that mast cell activation occurs during rhinovirus infections.
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PMID:Mediators of immediate hypersensitivity in nasal secretions during natural colds and rhinovirus infection. 609 51


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