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)

In some persons, cold, dry air (CDA) provokes symptoms of rhinitis that are associated with increased levels of histamine and other inflammatory mediators in nasal lavages. Because the patterns of mediators released during the early reaction to antigen and CDA-induced rhinitis are similar, we believe that mast cell activation is part of the reaction to CDA. In view of our previous finding that 1-wk pretreatment with topical steroids reduced symptoms and mediator release in the early nasal response to antigen of allergic subjects, we examined the effect of beclomethasone dipropionate on the response to CDA. Using a double-blind, crossover design, 84 micrograms of beclomethasone or placebo were administered in each nostril twice a day to 13 volunteers for 7 days prior to CDA challenge. The reaction to CDA was monitored by measuring the levels of histamine, N-alpha-p-tosyl-L-arginine methyl ester (TAME)-esterase activity and albumin in nasal lavages before and after provocation. Overall symptom scores, as well as scores for rhinorrhea and congestion, were also obtained. Cold, dry air challenge resulted in elevation over baseline of all parameters after placebo pretreatment. After beclomethasone, a significant reduction in histamine levels, but not in TAME-esterase activity or albumin levels or in number of symptoms, was observed. These results indicate that 1-wk pretreatment with beclomethasone affects mast cells, reducing histamine release after CDA, as it did in antigen-induced rhinitis. They also indicate that histamine may not be essential for the development of the immediate nasal reaction to CDA.
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PMID:Steroid-induced reduction of histamine release does not alter the clinical nasal response to cold, dry air. 170 10

A defective histaminergic dilating system in the digital vasculature has been proposed for the pathophysiology of Raynaud's phenomenon but this is not supported by studies of digital intradermal responses to histamine or agents which cause histamine release. The vascular responses (measured by planimetry and laser Doppler flowmetry) of digital skin over the middle phalanx to intradermal histamine, compound 48/80 and Substance P have now been studied at low temperatures (because it is in the cold that Raynaud's phenomenon occurs) in normal controls and patients with primary Raynaud's phenomenon. A cold-related attenuation of mast cell histamine release by compound 48/80 was observed in both normal and Raynaud's subjects. These results do not support a major histaminergic defect in the pathogenesis of Raynaud's phenomenon.
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PMID:Vascular responses to histamine at low temperatures in normal digital skin and Raynaud's phenomenon. 171 28

The bladder mast cell contains many granules, each one of which can secrete many vasoactive and nociceptive molecules. A number of conditions such as extreme cold, drugs, neuropeptides, stress, trauma, toxins, etcetera, can trigger the mast cell to secrete some of its contents. In turn, these chemicals can sensitize sensory neurons, which can further activate mast cells by releasing neurotransmitters or neuropeptides. Additionally, the mast cell can directly cause vasodilation and bladder mucosa damage while attracting inflammatory cells, thus causing many of the problems observed in IC. Clinicians may be at a distinct disadvantage because they are faced with a multitude of potential mast cell triggers and numerous mediators secreted. Therefore, it may be advisable to block or inhibit the mast cell from responding to many of these various stimuli. Specific mast cell mediators should be assayed as possible diagnostic tools, whereas potential inhibitors of mast cell secretion should be tried under controlled conditions to determine the extent of therapeutic benefit.
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PMID:Bladder mast cell activation in interstitial cystitis. 185 17

The present study investigates the contribution of gastric mast cells on PGD2 generation in rat gastric mucosa. Cold-restraint induced stress or i.v. carbachol injection methods were used for gastric mast cell degranulation. In 19 stressed, 15 carbachol-infused and 14 control rats, gastric mast cell counts and gastric mucosa PGD2 assay were performed. Gastric mucosal content of PGF2 alpha was also determined in carbachol infused and control rats. The mean number of gastric mast cells was significantly lower in stressed and carbachol infused than in control rats. Despite these differences in gastric mast cell counts, neither PGD2 or PGF2 alpha contents in the gastric mucosa were significantly different in mast cells degranulated rats than in control animals. These results suggest another source of PGD2 in the rat gastric mucosa other than mast cells.
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PMID:Mast cells in the rat gastric mucosa are not primarily responsible for PGD2 generation. 187 77

Zinc compounds have been shown to antagonize various types of gastric ulceration in rats. Zinc carnosine (Z-103), a newly developed agent was, therefore, examined for its antiulcer effect in stress-induced ulceration and also its membrane stabilizing action in rat stomachs. Cold-restraint (restrained at 4 degrees C for 2 h) stress induced severe hemorrhagic lesions together with increased mast cell degranulation and beta-glucuronidase release in the gastric glandular mucosa. Z-103 pretreatment with a single oral dose (3, 10 or 30 mg/kg) reversed these actions in a dose-dependent manner. When the compound was incubated in concentrations of 10(-7, 10(-6), 10(-5) or 10(-4) M, with isolated hepatic lysosomes, it significantly reduced the spontaneous release of beta-glucuronidase in the medium. The present study not only demonstrates the antiulcer effect of Z-103 but also indicates that the protective action is likely to be mediated by its membrane-stabilizing action on mast cells and lysosomes in the gastric glandular mucosa.
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PMID:The membrane-stabilizing action of zinc carnosine (Z-103) in stress-induced gastric ulceration in rats. 194 72

A group of 187 asthmatics that had been using corticotherapy for at least a year was studied to ascertain the actual necessity of this treatment as well as the clinical and etiologic forms of bronchial asthma in these patients. Thus 3 categories of patients could be delineated; 112 patients with total (permanent) corticodependence, 25 patients with transient (seasonal) corticodependence and 50 patients with pseudocorticodependence. Generally, the category with total corticodependence consisted of patients with intrinsic asthma or with confirmed polyintricated allergic asthma. The criteria for inclusion in this category were: lack of response to bronchodilating treatment, estimated clinically and by FEV1 and/or Raw (resistance of air ways) determinations, and impossibility to achieve corticotherapy "sevrage" by associating mast cell-degranulation inhibitors (ketotifen and/or disodium chromoglycat--DSCG). In the other two categories corticosteroid sevrage could be achieved either transiently in the case of the second category (corticodependent patients only in the warm season--asthmatics with allergy to pollens, resistant to the usual treatment--or in the cold season--some asthmatics with infectious trigger) or completely in the patients of the third category (with pseudocorticodependence). In these latter subjects (about a quarter of the patients with prolonged corticotherapy), mostly asthmatics with ignored allergic etiology, the etiologic approach of disease and the association of Ketotifen and/or DSCG led to disappearance of corticodependence.
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PMID:Contribution to the study of the etiopathogenic and background peculiarities in patients with corticodependent bronchial asthma. Note I. Concepts of corticodependence and pseudocorticodependence. 194 11

Nicotine 5, 25 or 50 micrograms/ml drinking water given ad lib for 5, 10 or 20 days, dose- and time-dependently worsened cold-restraint-induced (stress) ulceration in rat stomachs. Treatment with nicotine 5 or 25 micrograms/ml did not influence the number of gastric mucosal mast cells degranulated by cold and restraint; however, drinking 50 micrograms/ml for 10 days lowered further the mast cell count in stressed animals. During 20-day nicotine administration, the daily food intake and body weight gain, up to the 18th day when the animals were starved before experiments, were not affected by the three concentrations of the alkaloid, except that fluid consumption tended to be less only in those animals given the highest dose. The findings indicate that chronic nicotine treatment exacerbates the severity of stress-evoked ulcer formation. The ulcer-intensifying mechanism of the two lower doses of nicotine appears not to be related to additional mast cell degranulation; only the ulcerogenic action of the highest concentration includes this factor. It is unlikely that ulcer aggravation by nicotine is due to malnutrition because body weight gain and solid food intake by the alkaloid-treated rats were normal.
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PMID:Chronic nicotine treatment intensifies gastric ulceration by cold-restraint stress in rats. 195 Aug 22

The effects of sulphasalazine and of its major constituents, sulphapyridine and 5-aminosalicylic acid (5-ASA), on gastric ulceration as well as on changes in mast cell counts and mucus levels in the glandular mucosa were examined in restrained rats exposed to 4 degrees C (stress) for 2 h. Sulphasalazine (50, 100, 200 mg/kg), sulphapyridine (31.25, 62.5, 125 mg/kg) or 5-ASA (18.75, 37.5, 75 mg/kg) was injected subcutaneously 0.5 h before stress induction. Cold-restraint stress produced gastric glandular mucosal ulcers which were significantly reduced by all three doses of sulphasalazine and the higher doses of sulphapyridine and 5-ASA. Sulphasalazine prevented mast cell degranulation and increased the amount of mucus adhering to the mucosa. In contrast, the higher doses of sulphapyridine significantly increased only the mucus levels, whereas those of 5-ASA effectively prevented mast cell degranulation. The results show that the total effect of sulphasalazine is approximately equivalent to the summation of the actions of its component doses of sulphapyridine and 5-ASA. It is notable that sulphapyridine itself appears to be biologically active in reducing ulcer severity.
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PMID:Inhibition of stress-induced gastric ulcers by sulphasalazine and its constituents (sulphapyridine and 5-aminosalicylic acid) in rats. 197 55

The effects of nifedipine and cimetidine on cold/restraint stress-induced gastric ulcers and glandular wall mast cell count were studied in rats. Two hours of restraint at 4 degrees C resulted in 90% ulceration rate in the glandular stomach with a decrease in glandular wall mast cell count in the mucosa, submucosa and muscle layer. Nifedipine in three doses (1, 5 and 10 mg/kg) administered i.p. 30 min before stress significantly and dose dependently prevented gastric ulceration and mast cell degranulation. Cimetidine, in doses of 50, 100 and 150 mg/kg, again administered 30 min before stress prevented only gastric ulceration dose dependently without a significant change in mast cell count. The results indicate that both nifedipine and cimetidine are equally effective to reduce gastric mucosal ulceration in response to stress. However, the unique effect of nifedipine to inhibit mast cell degranulation which was now clearly demonstrated may favour the potential value of this drug in the management of peptic ulcer disease in humans.
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PMID:Nifedipine versus cimetidine in prevention of stress-induced gastric ulcers in rats. 204 Mar 56

Inhaled furosemide has been recently demonstrated to inhibit the bronchoconstrictive effects of exercise, ultrasonically nebulized distilled water, and antigen challenge. The presumed mechanism of action of these challenges is through mast cell degranulation. We report on the effect of inhaled furosemide on cold-air hyperventilation challenge (CAHC) and methacholine challenge. We studied 10 subjects with mild to moderate asthma in a double-blind, placebo-controlled, crossover study. Inhaled furosemide did not affect FEV1 in the hour after inhalation, and there was no significant difference between placebo or furosemide on the dose of methacholine causing a 20% fall in FEV1. Our results demonstrated inhaled furosemide significantly attenuated the bronchoconstrictive effect at 6 and 9 minutes after CAHC (p less than 0.05 and 0.029, respectively) when furosemide was compared to placebo and approached significance at 12 and 15 minutes after CAHC (p = 0.052 and 0.56, respectively). Inhaled furosemide attenuates CAHC but does not effect methacholine-induced bronchoconstriction.
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PMID:Effect of inhaled furosemide on the bronchial response to methacholine and cold-air hyperventilation challenges. 233 65


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