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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The test of indirect degranulation of rat mast cells was applied to the study of the specific activity of 16 series of noninfectious allergens from domestic dust (3 series) from hotel dust (7 series) and from the pollen of fescue (6 series). The concentration of protein nitrogen in the allergens from the domestic and hotel dust constituted to 10 000 PNU, and in the allergen from the pollen of fescue--125 000, 50 000, 15 000 and 7 000 PNU. In studying the specific activity of domestic allergens use was made of the sera of patients suffering from bronchial asthma with a marked allergy to domestic dust sera of patients with pollinoses with a marked allergy to fescue pollen was applied to the study of the specific activity of pollen allergen. For the assessment of the indirect degranulation test in mast cells of rats an index of mast cell degranulation of rats (IMCDR) was employed. It was shown that the IMCDR values were equal to 0.46, 0.58, 0.62 in using the domestic dust and in the case of the hotel dust - from 0.17 to 0.28. The mean values for the group of preparations from the domestic dust were 2.5 times greater than for the group of preparations for the hotel dust and were 0.55 and 0.22, respectively. For the allergen from the fescue pollen the IMCDR values varied from 1.23 to 0.16, and increased with the rise of the protein nitrogen concentration (PNU). Additional studies demonstrated that the specific activity of the domestic dust allergen with the crude sera and with those preserved in frozen condition for 3 to 6 months was almost the same. The results obtained permit to draw a conclusion that the method of indirect degranulation of rat mast cells with trizing of commercial batches of infectious allergens.
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PMID:[Use of the indirect rat mast cell degranulation reaction in vitro for characterization of the specific activity of non-infectious allergens]. 6 80

IgE is a homocytotropic antibody which binds to the surface of the mast cell. Antigen with affinity for IgE triggers conformational change at the cell surface, resulting in the release of chemical mediators from the mast cell granules. The mediators histamine, slow reacting substance of anaphylaxis and eosinophil chemotactic factor cause smooth muscle contraction, increased capillary permeability, eosinophil attraction and increased glandular secretions. The release of mediators from the mast cell granules is controlled by intracellular levels of cyclic nucleotides. In particular, elevated cyclic AMP inhibits mediator release. Adrenergic, cholinergic and prostaglandin receptors all influence mediator release. The characteristic immunopathology of immediate hypersensitivity reactions is a result of local or systemic mediator release. Such reactions include anaphylaxis, asthma, allergic rhinitis, urticaria and angioedema. Similar immunopathology may sometimes result from mechanisms not involving IgE or histamine mediators. Routine investigation of patients with immediate hypersensitivity should include eosinophil counts and IgE levels in blood and secretions, and immediate hypersensitivity skin tests. RAST testing is not routine. Therapeutic principles of these reactions include restoration of inhibitory levels of cyclic nucleotides, antagonism of mediator effects and immunological manipulation of the IgE mediated allergic reaction.
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PMID:The immunological basis of immediate hypersensitivity. 8 47

Pyridoxine, one of the B vitamins, has been shown to be useful in the treatment of childhood bronchial asthma by Collip et al. (1975). A double-blind study with 76 asthmatic children followed for five months indicated significant improvement in asthma following pyridoxine therapy (200 mg daily) and a reduction in dosage of bronchodilators and cortisone. Other reports have shown that nicotinamide, another B vitamin shows inhibitory activity in rat mast cell degranulation and histamine release (Bekier et al. 1974, Wiczolkowska and Maslinski, 1975, 1976). These results induced us to investigate if pyridoxine, like nicotinamide or disodium cromoglycate, exhibits pharmacological inhibitory activity in rat mast cell degranulation and histamine release induced by antigen or other non-immunological stimulants. We found that pyridoxine at concentrations of 10 (-3) M, or greater significantly inhibited rat mast cell degranulation and histamine release induced by phospholipase A, compound 48/80, antigen (egg albumin) or a mixture of dextran and phosphatidyl serine, respectively. In these experimental models, pyridoxine shows a pharmacological profile similar to nicotinamide and disodium cromoglycate, although weaker than the latter. In spite of this, the lack of toxicity of this vitamin at relatively high doses (1 or 1.5 g), the possibility that other mechanisms of action may be involved, such as the improvement in tryptophan metabolism reported by Collip following pyridoxine therapy, suggest that this vitamine merits additional research.
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PMID:[Effect of pyridoxine on histamine liberation and degranulation of rat mast cells]. 9 42

Cromolyn is a prototype of a new series of drugs, the pharmacologic activities of which may offer an entirely new approach in the treatment of asthma. Whereas bronchodilator drugs and steroids act primarily at tissue sites to counteract the effects of various toxic mediators released from tissue mast cells, cromolyn prevents the release of such mediators from mast cell membranes. The advent of cromolyn sodium therapy has been recognized as a significant advance by the pharmaceutical industry, which is rapidly developing a series of cromolyn-like drugs with similar properties. Many of these compounds are active orally, and some preliminary investigations suggest that they also could be clinically effective. Cromolyn has therapeutic value in immunologic and nonimmunologically induced bronchospasm, being particularly suited for conditions amenable to long-term prophylactic therapy. The risk-to-benefit ratio of cromolyn sodium therapy is excellent. Cromolyn sodium is an important adjunct in the treatment of asthma. By topical administration the drug has been effective in seasonal and perennial rhinoconjunctivitis and in selected cases of gastrointestinal allergy to foods.
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PMID:Therapy with cromolyn sodium. 9 84

In an attempt to elucidate the mechanisms involved in analgesic-induced asthma, I performed bronchial and intravenous challenge tests with indomethacin in 5 aspirin-sensitive asthmatics. Bronchial challenge with less than 2 mg of indomethacin elicited bronchoconstriction that developed immediately in most cases, reached its macimum at a mean time of 64 min, and was over within 2 to 4 h. The time sequence of the reaction after intravenous challenge was similar to that after bronchial challenge, except that to obtain a comparable degree of bronchoconstriction it was necessary to administer at least twice the inhaled dose. Inhalation of disodium cromoglycate during bronchoconstriction inhibited the reaction within 8.6 +/- 5.7 min, regardless of the route of challenge. This suggests that sequential mast cell degranulation with liberation of chemical mediators is the mechanism responsible for bronchoconstriction in analgesic-induced asthma.
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PMID:Bronchial and intravenous provocation tests with indomethacin in aspirin-sensitive asthmatics. 11 81

Guinea pigs were exposed to aerosols of histamine or the mast cell degranulating and histamine releasing substance 48/80. Cromolyn sodium aerosols prevented 48/80 induced asthma but did not influence histamine induced broncho-constriction. 48/80 given daily for 5 days resulted in marked decrease in susceptibility to 48/80, possibly because of depletion of histamine and other active substances. There was no change in histamine sensitivity. After 3 days of rest, normal susceptibility to 48/80 returned.
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PMID:Effect of cromolyn sodium and of daily exposure to compound 48/80 on experimental asthma. 23 45

Nothwithstanding difficulties associated with the limitations of survey techniques and methodology employed to define asthma, the evidence accumulated to date suggests that the reported differences in the prevalence rates of this disease from country to country and within local populations of the one country are real. It is accepted that allergy is not the sole cause of asthma but nonetheless hypersensitivity to environmental allergens is a significant triggering factor in most countries of the world. Comparisons between countries might therefore be influenced by the time of the year when the survey is taken since the prevalence of seasonal asthma would be higher in the period of pollinosis. Environmental factors, and in particular the relative atmospheric concentrations of pollens and the density of house dust mite (D. pteronyssinus and D. farinae) in dwellings, must therefore be considered when accumulating prevalence data. The prevalence rate for childhood asthma is high in Australia, United Kingdom, United States of America and New Zealand, and medium to low in the Scandinavian countries and Switzerland. It is not clear what factors contribute toward these differences since several studies indicate that racial characteristics per se are not pre-eminent in defining susceptibility to asthma. Most surveys indicate that the prevalence of childhood asthma is low to very low among low-income populations living in tropical areas. While it is possible to implicate inadequate diagnosis, genetic factors, nutritional status and allergen exposure as factors contributing towards the low prevalence, it has become fashionable to attribute this observation to the influence of certain helminthic infections. Parasites stimulate the production of high levels of serum IgE, the bulk of which has as yet an undetermined specificity. The suggestion that this IgE blocks mast cell receptors leaving insufficient sites available for sensitization by allergen-specific IgE antibody is attractive. However, since the kinetics of binding to mast cell receptors is unlikely to be the same for all IgE molecules, irrespective of their specificity, this hypothesis appears to be an oversimplification of the problem. It is more likely that parasitic infections repress the synthesis of IgE antibody to environmental allergens, although the mechanism for this is unclear. Circumstantial evidence suggests that the time course of exposure to parasites versus sensitization by environmental allergens may be critical. Another possibility is that parasitic infections in some way nullify the effect of allergens at the level of the target organ, perhaps through the modulating role of eosinophils. If it is established that parasitic infections, particularly in early childhood, suppress the capacity of potentially atopic children to develop asthma and other allergic disorders, there would be some justification in attempting to circumvent allergic disorders in susceptible individuals by a harmless preparation of parasite antigens.
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PMID:The conflicting role of parasitic infections in modulating the prevalence of asthma. 28 88

1 Cinnarizine, an inhibitor of calcium ion transport across smooth muscle cell membrane, has been shown to exert an anti-asthmatic effect in patients with chronic asthma. 2 It is postulated that antagonism to calcium ion transport across the mast cell membrane may cause the compound to have a pharmacological effect similar to sodium cromoglycate. 3 Cinnarizine is orally active and its therapeutic effect is demonstrated in a double-blind, cross-over, placebo controlled study. 4 Patient benefit was shown by a significant improvement in peak flow rate. A non-significant trend towards a reduction in symptomatic bronchodilator usage and a decrease in asthma symptom score was also shown. 5 It is concluded that cinnarizine could well prove to be the first of a new family of anti-asthmatic drugs offering a protective effect when taken systemically.
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PMID:Cinnarizine in the treatment of chronic asthma. 36 14

Five patients with asthma and severe aspirin hypersensitivity were challenged on separate days with increasing doses of aspirin given by mouth, starting with 5 mg, until a reduction in FEV1 greater than 15% was obtained. Sodium cromoglycate in doses of 20-40 mg inhibited the bronchoconstrictive reaction not only when inhaled before the challenge but also after it, at a time when progressive reduction in FEV1 values was taking place. According to these results, it seems reasonable to postulate sequential mast cell degranulation and liberation of mediators of anaphylaxis as the mechanism through which aspirin induces bronchoconstriction in aspirin-sensitive asthmatics. The differences between bronchial provocation tests and oral challenge with aspirin are stressed.
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PMID:Inhibition of aspirin-induced bronchoconstriction by sodium cromoglycate inhalation. 41 71

This study describes the histopathology and ultrastructure of bronchial mucosa in lung biopsies from two children with bronchial asthma in remission, and compares them with lung samples from two children who died in status asthmaticus. Light microscopy of all samples showed changes typical of bronchial asthma, e.g. mucus plugging, goblet cell hyperplasia, 'thickening of bronchial basement membrane', peribronchial smooth muscle hypertrophy and eosinophilic infiltration. Electron microscopy revealed that the mucus plugs consisted of moderately electron-dense floccular material containing degenerate epithelial cells, macrophages and cell fragments. The luminal surfaces of ciliated cells showed cytoplasmic blebs and abnormal cilia. Mast cells in various stages of degranulation were scattered between bronchial epithelial cells. The subepithelial hyaline layer, commonly referred to as "thickened basement membrane", consisted of collagen fibrils in plexiform arrangement. The basement membrane proper appeared intact. These electron microscopic changes, particularly the presence of mast cells and subepithelial collagen deposits, were also found in autopsy samples. This combined light and electron microscopic study shows that marked, possibly irreversible changes may be present in the lungs of patients with severe bronchial asthma, even when they are asymptomatic. These pulmonary changes could be the direct consequence of mast cell activation and the release of various mediators. No evidence of immune complex deposition was found.
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PMID:Ultrastructure of airways in children with asthma. 1240 26


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