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)

A nasal challenge model of allergic rhinitis was used to determine if pretreatment with oral theophylline reduces histamine release in vivo. Ten subjects were entered into a double-blind, cross-over trial. The results showed that both the physiologic response (sneezing) (p = 0.02) and the amount of mediators (histamine, kinins, toluene sulfonyl arginine methyl ester esterase activity) (p less than 0.01 for all) released into nasal secretions were significantly reduced after one week of pretreatment with theophylline. At the time of challenge, the serum concentrations of theophylline were between 8 and 22 micrograms/ml. It is speculated that the ability of theophylline to block the clinical response to antigen challenge and to decrease the release of mast cell mediators contributes to its clinical efficacy in the treatment of asthma.
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PMID:Theophylline reduces the response to nasal challenge with antigen. 241 77

When peritoneal resident cells (PRCs) of genetically mast cell-deficient WBB6F1-W/Wv mice were cultured in vitro for 5 h at 37 degrees C, their histidine decarboxylase [HDC, L-histidine carboxylase, E.C. 4.1.1.22] activity increased 10-fold. Since inhibitors for energy production and mRNA and protein syntheses inhibited this increase of HDC activity, it appeared to represent de novo synthesis of the enzyme, i.e., induction. This increase was followed by an increase in the amount of histamine in the culture medium of the cells, indicating that histamine synthesized by the induced HDC was not stored in the cells but was quickly released. Mast cells were not involved in the HDC induction, because the extents of HDC induction in PRCs of W/Wv and wild type +/+ mice were similar. The removal of T cells with anti-Thy-1,2 antibody and complement from the PRCs did not affect the HDC induction, but the removal of phagocytes decreased the induction to one-tenth in spite of a 2-fold increase in the proportion of B cells in the PRCs. After separation of the PRCs into adherent and non-adherent fractions, the increase in HDC activity was found to be associated with the adherent fraction that was mostly positive to esterase staining. These results suggest that HDC was induced in peritoneal macrophages.
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PMID:In vitro increase of histidine decarboxylase activity and release of histamine by peritoneal resident cells of mast cell-deficient W/Wv mice; possible involvement of macrophages. 245 55

A double blind, placebo-controlled, cross-over study was performed to determine the effect of cetirizine, an H1 antihistamine, on the immediate nasal allergic response. Ten persons underwent nasal challenge with antigen after premedication with 20 mg of cetirizine or placebo QD for 2 days. The response was monitored by counting the number of sneezes and by measuring the levels of histamine, prostaglandin D2, leukotriene C4, albumin, and TAME-esterase activity in recovered nasal lavages. The results showed a significant reduction in sneezing and in the amounts of recovered albumin, TAME-esterase activity, and leukotriene C4 but no reduction in the amounts of recovered histamine and prostaglandin D2. These results suggest that cetirizine does not inhibit mast cell activation but inhibits the consequences of the released histamine on H1 receptors: sneezing and increased vascular permeability. The results further suggest that mast cell release of histamine is the direct result of antigen stimulation, as opposed to reflex activation, and that other cells in addition to mast cells generate leukotrienes during the early allergic response.
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PMID:The effect of cetirizine on early allergic response. 256 79

To increase understanding of the effect of H1 antihistamines on the immediate response to nasal challenge with antigen, we performed two double blind, placebo-controlled, crossover studies using cetirizine and terfenadine. The subjects underwent nasal challenge with antigen after premedication with either cetirizine (20 mg QD for two days, n = 10), terfenadine (60 mg BID for 1 week, n = 12), or placebo for equivalent periods of time. We monitored the response to challenge by counting the number of sneezes and by measuring the levels of inflammatory substances in recovered nasal lavages. Compared with placebo, both antihistamines significantly reduced sneezing and the levels of recovered albumin and TAME esterase activity, suggesting that both reduced the expected increase in vascular permeability. With cetirizine, there was also a reduction in the levels of LTC4 (not measured in terfenadine studies) but not in those of recovered histamine and prostaglandin D2. These data suggest that cetirizine did not affect mast cell mediator release, that histamine release is due to the direct action of antigen stimulation and that leukotrienes are generated by cells in addition to mast cells. With terfenadine, there were significant reductions in the levels of histamine and kinins (not measured in cetirizine study) seen after nasal challenge with antigen. The reduction in kinins most likely reflects alteration in vascular permeability, whereas the effect on histamine presumably reflects inhibition of mast cell activation. When combined, these experiments demonstrate effects of H1 antihistamines on histamine release beyond those usually described, as well as differences between drugs within a single classification.
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PMID:The effects of H1 antihistamines on the early allergic response. 257 50

Bone marrow-derived leukocytes of murine epidermis can express two phenotypes: typical Langerhans cells, which are Ia+ and Thy-1-, and a recently discovered second population that is Thy-1+ and Ia-. To verify that these phenotypes are expressed by two different cell types, and to help understand their lineage and function, we have studied morphology and reactivity with a large panel of antibodies. Dual antibody immunofluorescence combined with electron microscopy showed that Thy-1+ and Ia+ cells were each distributed in a regular fashion and formed adjacent dendritic systems in or close to the basal layer. Double-labeling studies with anti-Ia and a second monoclonal antibody revealed that all Langerhans cells expressed F4/80 (macrophage), Mac-1 (C3bi receptor), and 2.4G2 (Fc receptor), as well as the thymus leukemia (TL) and heat-stable (M1.69/16) antigens. A large fraction expressed S100 and all exhibited membrane ATPase and nonspecific esterase. In contrast, Thy-1+ cells lacked all these features of Langerhans cells, except that a minority were strongly reactive with 2.4G2. Thy-1+ cells also lacked differentiation antigens of most other types of leukocytes, except they were rich in asialo GM1. By electron microscopy, Thy-1+ cells had cytoplasmic granules that were similar in structure and in their aryl sulfatase content to those previously described in natural killer cells. The granules were enlarged in beige mice, suggesting a lysosomal origin, and were present in mast cell-deficient W/Wv mice, indicating no relation to mast cells. We conclude that Thy-1+ epidermal cells are thoroughly distinct from Langerhans cells. On the basis of morphology and phenotype, they may represent a type of tissue natural killer cell. Thy-1+ natural killer cells are now being identified in several nonlymphoid sites, such as gut epithelium and the livers of mice given adjuvants. If Thy-1+ epidermal cells prove to be natural killer cells, it is noteworthy that they represent a resident population regularly distributed in the basal layer of all mouse strains. The notion that Thy-1+ epidermal cells are immature natural killer cells is intriguing in light of recent evidence that Ia+ Langerhans cells are also immature with respect to accessory cell function. The epidermis may not have the functional capacities of a lymphoid organ, but it could contribute immature cells important for both natural and acquired resistance.
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PMID:The Thy-1-bearing cell of murine epidermis. A distinctive leukocyte perhaps related to natural killer cells. 286 Dec 45

Myofiber injury-repair was studied in rat soleus muscles to elucidate the role of infiltrating cells in the injury-repair process. Muscle injury was induced by forced muscle lengthening with the contralateral muscle serving as a control. The muscles were removed for histologic, histochemical and immunohistochemical procedures at varying periods (12-120 h) post-injury. All injured muscles were severely damaged with many cells present in the interstitial spaces between myofibers. Normal appearing myofibers demonstrated elevated lysosomal proteolytic activity, but no evidence of increased activity, indicative of phagocytic cells, was found in or between damaged myofibers. The esterase stain for macrophages and immunohistochemical techniques for mast cells also provided no support for either cell type predominating in the damaged area, although mast cell degranulation could be observed in the pericapillary regions. In contrast, the use of a specific antisera for a multicatalytic protease uniquely defined most of these cells as myogenic in origin. They appeared to be most numerous between the torn ends of a myofiber. Surprisingly, the remainder of the cells appeared to be of lymphoid origin.
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PMID:Characterization of muscles injured by forced lengthening. I. Cellular infiltrates. 305 Mar 53

A mast cell granule proteinase was purified from isolated ovine mucosal mast cells by cation exchange chromatography, which defined the conditions for enzyme purification from sheep gastric mucosae. Antibodies raised against the proteinase were used in subsequent purification procedures which yielded 78 micrograms of enzyme per 5 g wet wt of abomasal tissue. Immuno-histochemistry confirmed that mucosal mast cells were the source of the enzyme. The proteinase had chymotrypsin-like esterase activity, with a molecular weight between 19,000 and 25,000.
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PMID:The isolation and purification of a proteinase with chymotrypsin-like properties from ovine mucosal mast cells. 309 19

There is little or no direct in vivo evidence in man to support the involvement of mast cell-mediator release in the pathogenesis of immediate allergic reactions. We have performed a within-subject controlled study to determine the changes that occur in nasal mast cells during allergen-induced rhinitis. Twelve subjects with asymptomatic rhinitis were studied. Nasal biopsy specimens were obtained from each subject after a control solution (isotonic saline, 0.9% w/v) had been nebulized into one nostril and allergen solution (freeze-dried allergen extract reconstituted with isotonic saline) into the other. The tissues obtained were fixed in Carnoy's solution and stained with the alpha-naphthol AS-D chloroacetate esterase reaction (N AS-D CA ER). Mast cells were counted under light microscopy in the epithelium and lamina propria, and the integrity of each cell was assessed. No significant differences were found in the number of epithelial or lamina propria mast cells in biopsy specimens obtained after saline or allergen administration. However, the number of degranulated mast cells after allergen provocation (89%) was significantly greater than after instillation of control solution (15%) (p = 0.003). Changes of mast cell degranulation after allergen provocation were confirmed by electron microscopy. In six nonatopic, control subjects without rhinitis, there was no significant difference between the percentages of degranulated mast cells after allergen provocation (25.8%) and instillation of saline (24.3%). This study provides direct in vivo evidence for allergen-induced mast cell activation in man.
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PMID:Direct in vivo evidence for mast cell degranulation during allergen-induced reactions in man. 309 10

In order to assess the role of arachidonic acid metabolites in the early reaction to antigen, we challenged six allergic individuals with and without premedication with aspirin and recorded their clinical response, as indicated by number of sneezes, and measured the levels of inflammatory mediators. The early reaction to antigen was associated with increases in the levels of histamine, N-alpha-tosyl-L-arginine methyl esterase (TAME-esterase) activity, prostaglandin (PG) D2, leukotriene C4, PGE, and thromboxane. Aspirin significantly inhibited the increases in the cyclooxygenase metabolites PGE, PGD2, PGF2 alpha, 6-keto-PGF1 alpha, and thromboxane but did not affect the amount of sneezing or the levels of histamine, TAME-esterase activity, or leukotrienes. The pattern of the metabolites and their response to pretreatment with aspirin parallel the response of purified human lung mast cells, supporting the notion that the early phase of allergic rhinitis is a mast cell-dominated event.
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PMID:Arachidonic acid metabolites during nasal challenge. 309 12

In chronic granulocytic leukaemia, hybridoid leucocytes can regularly be found. Light microscopically they contain a mixture of eosinophilic, basophilic and naphthol AS-D chloroacetate esterase-positive granules. The present study was done to clarify the ultrastructural composition of these cells. It could be clearly shown that in some leukaemic granulocytes primary and secondary eosinophilic as well as basophilic granules occur side by side. There were also basophils with additional tissue mast cell granules. Since normal mast cell granules as well as granules of normal eosinophilic promyelocytes are naphthol AS-D chloroacetate esterase-positive, it would appear possible that mastocytoid as well as primary eosinophilic granules within the leukaemic basophils are responsible for the atypical, granular naphthol AS-D chloroacetate esterase-positivity of these cells. The existence in chronic myeloid leukaemia both of mixed basophilic and eosinophilic granulated leucocytes and of mixed basophilic and mastocytoid granulated leucocytes may suggest a common myeloid precursor of eosinophils, basophils and tissue mast cells. In addition, the hybridoid granulocytes may be considered an expression of a neoplasia-related lineage infidelity.
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PMID:Electron-microscopic characterization of mixed granulated (hybridoid) leucocytes of chronic myeloid leukaemia. 316 78


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