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

The role of mast cell histamine in body reactivity of rats under experimental stressful conditions was studied. Animals submitted to chronic anaphylactoid reactions (by injecting compound 48/80 at the dose of 1 mg/kg, i.p., twice daily, for five days), when exposed to cold-restraint stress, exhibited a fully evident inflammatory response in the carrageenin-oedema test, whereas saline-treated rats, under the same experimental conditions, showed reduced paw oedema. Interestingly, a single injection of compound 48/80 increased the pituitary content of Beta-endorphin(ir), but chronic administration failed to produce this effect suggesting that some adaptation of the organism to repeated anaphylactoid reactions may occur. These results support the hypothesis of correlations between pituitary Beta-endorphin and mast cell histamine in the reactivity of the organism to stressful stimuli.
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PMID:Correlations between histamine and opioid peptides on the modulation of inflammatory processes in rats exposed to stress. 296 76

Nasal lavage after antigenic and nonantigenic nasal stimulation has become an important tool for the study of inflammatory phenomena in the upper airway. Biochemical and cytologic information is relatively easily obtainable, and pharmacologic manipulations can be readily monitored. This article is of several studies aiming toward a more profound understanding of the mechanisms of allergic and nonallergic rhinitis by the use of laboratory-challenge procedures and nasal-lavage techniques. An early and a late reaction are detected clinically in the nose after antigen challenge of allergic individuals. In addition, the sensitivity to antigen significantly increases after the initial challenge, and this phenomenon is not obligatorily linked to the presence of a late-phase reaction (LPR). Inflammatory mediators, mostly mast cell- and/or basophil-derived, are detected in the nasal washes and correlate with the symptomatology in both the early and the late reactions. The allergen-induced LPR is marked by an early influx of eosinophils and, later, basophils and neutrophils. Elevation of major basic protein and histamine, but not prostaglandin D2, is detected during the LPR, giving evidence of active eosinophil and basophil participation. Systemic steroids can effectively suppress the clinical, biochemic, and cellular manifestations of antigen-induced LPR. Topical steroids have a similar effect but are also capable of suppressing the early reaction to antigen. A nonallergic form of rhinitis can be induced in the laboratory by nasal inhalation of dry air at freezing temperatures in individuals who report sensitivity to cold and windy environments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies on the allergic and nonallergic nasal inflammation. 328 18

Kinins are generated in nasal secretions during allergic reactions and during induced rhinovirus colds. To determine if kinins may contribute to the symptomatology of these inflammatory reactions, 8 subjects were challenged with increasing doses of bradykinin or with placebo. Levels of albumin, histamine, and N-alpha-tosyl-L-arginine methyl ester (TAME)-esterase were measured in nasal lavages, and symptom scores were noted. No symptoms or increases in mediators or protein were observed after placebo challenge. Symptom scores increased in a dose-dependent manner, however, in response to bradykinin challenge. Increased symptoms were associated with significant increases in albumin and TAME-esterase activity, but no increases in histamine were observed. Nasal conductance measurements confirmed that bradykinin induces dose-dependent unilateral obstruction in the challenged nostril. Other common symptoms were rhinorrhea and, of particular relevance to rhinovirus infections, a persistent sore throat. We conclude that bradykinin causes increased vascular permeability and rhinitis, which are independent of mast cell mediator release. Kinins may, therefore, contribute to the symptomatology of inflammatory reactions of the upper airways, including the common cold.
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PMID:Nasal provocation with bradykinin induces symptoms of rhinitis and a sore throat. 334 41

The mechanism(s) by which repeated cold challenge in a patient with idiopathic acquired cold urticaria resulted in the induction of clinical tolerance to cold stimuli was studied. Plasma histamine levels, mast cell ultrastructure, and the cutaneous response to intradermal injections of morphine, histamine, and substance P were examined before and after the induction of tolerance. Plasma histamine levels draining cold-challenged, clinically tolerant skin were markedly diminished compared to histamine levels obtained during cold-induced angioedema. Furthermore, electronmicroscopy of skin samples taken from tolerant skin after cold challenge revealed intact, largely normal appearing mast cells. Intradermal injection of mast cell secretagogues and vasoactive agonists into normal and tolerant skin sites resulted in similar whealing responses. Thus, these studies suggest that the state of clinical tolerance to cold stimuli is due neither to mast cell-mediator depletion or tachyphylaxis of the cutaneous vasculature to vasoactive agonists. It appears likely that tolerance may be due to the induction of a specific state of unresponsiveness of mast cells to cold stimuli or possibly to depletion of a cold-induced cutaneous antigen capable of triggering mast cell degranulation.
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PMID:A case study on the induction of clinical tolerance in cold urticaria. 340 65

Recent evidence suggests that mast cell derived mediators other than histamine are likely to be involved in the pathogenesis of physical urticarias. Much of the work has been performed in idiopathic cold contact urticaria where the presence of neutrophil and eosinophil chemotactic factors, and platelet activating factor-like lipid substances have been previously demonstrated. Now, an increase in prostaglandin D2 measured by GC-MS has been demonstrated in venous blood draining the cold challenged area. This appeared a few minutes later than histamine, but then both substances paralleled the onset, development and subsidence of the urticarial reaction. There appeared to be no quantitative relationship between histamine and PGD2 release. A similar rise in histamine and PGD2 occurred on heat challenge of a subject with the rare localized form of heat urticaria. This rise of both substances was considerably reduced after combined treatment with induction of tolerance and oral indomethacin. The concentrations of PGD2 measured suggested that it plays an indirect role.
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PMID:[New pharmacologic developments in physical urticaria--therapeutic consequences]. 347 18

Enkephalins are a biochemical pathway for endogenous analgesia. A number of compounds inhibit degradation of enkephalins within the body. One of these compounds, D-phenylalanine (DPA), has been shown to increase the pain threshold in animals. It is hypothesized that this naloxone reversible analgesia is induced by DPA blockage of enkephalin degradation by the enzyme carboxypeptidase A. Preliminary studies of chronic pain patients have shown a response rate to DPA from 32% to 75%. This study was a double-blind crossover evaluation of a randomized parallel design to determine the efficacy of DPA in 30 subjects with chronic pain from varied etiology which was unrelieved by multiple therapeutic interventions. Each patient received a stabilized therapeutic regimen during this study consisting of four weeks of either DPA 250 mg or lactose (placebo) orally four times a day. After four weeks the DPA and placebo groups were crossed over for an additional four weeks of treatment. Pain was quantified using a visual analog pain scale and a cold pressor test. Data from the pain questionnaires revealed more pain relief on DPA reported by 25% of the patients, more pain relief on placebo reported by 22% of the patients, and no difference in pain relief reported by 53% of the patients. Lowest pain level of the visual analog scale was reported by 47% of the patients on DPA and 53% on placebo. There appears to be no significant analgesic effect from D-phenylalanine in chronic pain patients when compared to placebo.
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PMID:Analgesic effectiveness of D-phenylalanine in chronic pain patients. 352 9

We have used a model of nasal provocation to study the effects of pharmacologic interventions upon various types of inflammatory reactions of the upper airways. Pretreatment of allergic individuals with aspirin reduces the levels of prostaglandins in nasal secretions during the immediate allergic response but has no effect on symptoms. Theophylline and azatadine both reduce symptoms and the levels of mast cell mediators during the allergic response. By contrast, azatadine has no effect on symptoms or mediator levels during the response to challenge with cold, dry air, suggesting different mechanisms of mast cell activation in response to allergen and cold, dry air. Both topical and systemic steroids are effective in reducing symptoms and mediators during the late allergic response, but topical steroids also significantly inhibit the immediate response. Nasal challenge provides a convenient, relatively noninvasive method to study inflammatory reactions of the upper airways.
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PMID:Pharmacology of upper airways challenge. 357 May 20

The effects of zinc deficiency on gastric secretion and on cold-restraint stress-induced ulceration in rat stomachs have been studied. Administration of graded zinc deficient diets for 5 weeks significantly depressed the serum zinc concentration and decreased body weight gain in the rats. These diets significantly increased the gastric secretory volume, acid and pepsin. Zinc deficiency produced or aggravated the formation of glandular ulceration in the absence or presence of stress, respectively; it also decreased the mast cell count in the gastric glandular mucosa. It is concluded that zinc deficiency adversely affects the rats by reducing the body weight gain and producing ulceration which is probably mast cell-mediated. On the other hand, it increases gastric secretory functions.
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PMID:Zinc deficiency: its role in gastric secretion and stress-induced gastric ulceration in rats. 357 53

The effects of zinc acexamate on stress and reserpine ulcers as well as on gastric mast cells degranulation and membrane stability were evaluated in the rat. Zinc acexamate (100 mg/kg) has demonstrated an inhibitory effect on cold-restraint stress and reserpine-induced ulcer in a dose-dependent manner. Pretreatment of rats, prior to cold restraint stress, reduced gastric mast cell degranulation. Zinc acexamate (10(-4) M) inhibits Triton X-100 release of beta-glucuronidase in isolated hepatic lysosomes. These observations suggest that ulcer protective actions of zinc acexamate may be exerted in part through enhancing gastric mucosal resistance by stabilizing biological membrane integrity.
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PMID:Anti-ulcer and membrane stabilizing actions of zinc acexamate. 357 22

To determine whether morphological differences in the response of cutaneous mast cells characterize clinically distinct forms of urticaria, we used ultrastructural techniques to examine skin biopsy specimens from three patients with cold-induced urticaria and four patients with dermographism. Biopsy specimens were obtained before application of the stimulus and at the time of lesion formation. Patients with cold-induced urticaria exhibited morphological alterations only after stimulus application consisting of enlargement and uniform disorganization of some, but not all, granules, fusion of the membranes of adjacent granules, fusion of granule membranes with mast cell membranes, and discharge of electron-lucent and disorganized granule contents into the extracellular space. Mast cells from patients with immediate as well as delayed dermographism exhibited alterations before and after stimulus application consisting of enlargement of most granules, nonuniform (zonal) disorganization or solubilization of granule contents, fusion of granule membranes with mast cell membranes, and extracellular discharge of granule contents. Small cytoplasmic vesicles containing disorganized granular material were associated with the degranulation process. Endothelial cells lining nearby postcapillary venules exhibited prominent perinuclear condensation of contractile microfilaments during degranulation in both groups. Both before and after application of the stimulus, the walls of the superficial dermal vessels of the patients with dermographism were thinner and contained less extracellular matrix material than vessel walls of the patients with cold-induced urticaria. The morphologically distinctive types of mast cell degranulation that characterize these two clinically separable urticarial disorders may indicate different pathogenic mechanisms of lesion formation.
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PMID:Morphologically distinctive forms of cutaneous mast cell degranulation induced by cold and mechanical stimuli: an ultrastructural study. 366 25


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