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

We have previously reported highly potent basophil/mast cell (BMC) and basophil/eosinophil (Eo) colony-stimulating activities (CSA) in conditioned medium derived from cultured human nasal polyp epithelial scrapings (NP-CM). We now have examined the involvement of peripheral blood T-cells in the NP-CM stimulation of colony-forming units (cfu) from the blood of atopic and nonatopic subjects. Because the number of BMC- and Eo-cfu was significantly higher in cultures of peripheral blood from subjects with out-of-season ragweed allergic rhinitis than from control subjects (23.8 +/- 4.1 versus 9.0 +/- 2.4, p less than 0.01), we asked whether the observed colony stimulation could be a T-cell-dependent effect. Indeed, peripheral blood target cells consisting of a reconstituted mixture of T-cells and T-cell-depleted peripheral blood mononuclear cells (non-T-cells) yielded a significantly higher number of colonies in the presence of NP-CM than the non-T-cells alone. NP-CM did not stimulate colony formation by isolated T-cells. These observations point to interactions among nasal epithelial growth and differentiation factors, blood-borne progenitors and T-cells in the local accumulation of basophils, mast cells, and eosinophils in nasal polyps.
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PMID:Human nasal polyp epithelial basophil/mast cell and eosinophil colony-stimulating activity. The effect is T-cell-dependent. 246 80

Basophil leukocytes and tissue mast cells are inflammatory cells that are found in virtually all human tissues. They appear to be involved in the pathogenesis of such allergic diseases as allergic rhinitis, bronchial asthma, anaphylaxis, atopic and contact dermatitis, chronic urticaria, and hypersensitivity pneumonitis. By releasing a variety of chemical mediators, they could also play a role in the pathophysiology of a wide range of inflammatory disorders of the joints, and of intestine, lung, coronary, and myocardial diseases. Although these two cell types are similar in several aspects, striking differences have also been observed. Moreover, human mast cells from different anatomical sites and within an individual tissue synthesize different mediators and have different release mechanisms. The recent advent of techniques that yield highly purified basophils and mast cells from diverse tissues will probably lead to major advancements in understanding the biochemical and pharmacological mechanisms that control the release process of these cells. The release of mediators from these cells is also controlled by a series of largely undefined biochemical steps that represent the basis of the concept of basophil and mast cell releasability. Alterations of basophil or mast cell releasability have already been detected in patients with allergic rhinitis, bronchial asthma, atopic dermatitis, and chronic urticaria. Taken together, these findings demonstrate that basophils, mast cells, and their chemical mediators play a pivotal role in several inflammatory disorders.
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PMID:Pathophysiology of human basophils and mast cells in allergic disorders. 246 27

The vidian nerve provides the main parasympathetic nerve supply to nasal respiratory and maxillary sinus mucosa, and its electrical stimulation causes apparent secretory and vasodilatatory effects in animals. The present investigation was carried out in 8 patients with chronic hypertrophic non-allergic rhinitis (C.H.N.A.R.) undergoing therapeutic vidian nerve resection. The vidian nerve was electrically stimulated before the resection. Samples were taken from nasal sinus mucosa for histamine determination and microscopical observation before and after the stimulation period. Vidian nerve stimulation causes a significant decrease in histamine content and mast cell density in the mucosa sample, differentially influenced by eserine and atropine pretreatment.
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PMID:Histamine release from nasal mucosal mast cells in patients with chronic hypertrophic non-allergic rhinitis, after parasympathetic nerve stimulation. 246 76

Although theoretical considerations and experimental evidence implicate the mast cells in the pathophysiology of the immediate type hypersensitivity reaction, the evidence of their active participation in human allergic disease is still fragmentary. We have therefore sought evidence of mast cell activation in allergic mucosal disease using strictly seasonal allergic rhinitis as a model. Twelve patients with birch pollen-induced hay fever were examined before and well into the birch pollen season. Allergen exposure was monitored by pollen counts and the degree of symptoms registered daily. Small surgical biopsies and mucosal imprints were obtained from each patient before and during the season. Mast cells were analysed by light and electron microscopy and mucosal histamine was measured using a sensitive HPLC assay. We found a reduction in the number of mast cells in the nasal mucosa during pollen exposure (p less than 0.05) but no significant reduction of the histamine content. There was a correlation between the nasal mucosal mast cell density and histamine content before the pollen season (r = 0.76; p less than 0.01), but no such correlation was found during the period of pollen exposure (r = 0.19; n.s.). This finding points to secretory activity by the mast cells during the pollen season and to the appearance of a non-mast cell pool of tissue histamine. Evidence for a secretory activity of the mast cells during the pollen season was also confirmed by electron microscopy. In addition, we found a strong correlation (r = 0.77; p less than 0.01) between the histamine content of the nasal mucosa during the pollen season and the degree of nasal symptoms. The number of epithelium-associated mast cells found on mucosal imprints prior to the pollen season showed a strong correlation with the symptoms experienced later during the period of pollen exposure (r = 0.83; p less than 0.01). Taken together these observations indicate that the mast cell has a pathogenetic role in continuous allergic airway disease and re-emphasizes the role of histamine in the induction of the symptoms of allergic rhinitis.
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PMID:Secretory activity of nasal mucosal mast cells and histamine release in hay fever. 246 3

The clinical manifestations of allergic rhinitis are the result of an immune-mediated process after exposure of a sensitized individual to airborne allergens. The primary symptomatology includes nasal congestion, rhinorrhea, nasal and conjunctival pruritus, and sneezing. Principles of management include allergen avoidance, palliative therapy, immunotherapy, and pharmacotherapy. Oral decongestants stimulate alpha-adrenergic receptors in the nasal cavity, resulting in vasoconstriction and decreased edema. Oral antihistamines block histamine1 (H1) receptors, and may relieve rhinorrhea, sneezing, and nasal and conjunctival pruritus. Topical decongestants have a local effect on adrenergic receptors in the nasal mucosa, resulting in rapid, marked vasoconstriction. Intranasal corticosteroids inhibit mediator release from mast cells and basophils, and reduce edema of the nasal mucosa. Dexamethasone sodium phosphate, beclomethasone dipropionate, and flunisolide are currently available for intranasal administration. Cromolyn sodium inhibits allergen-induced degranulation and mediator release from sensitized cells, and is useful primarily as a prophylactic agent. Several agents, including the corticosteroids budesonide and flucortin butylester, the mast cell-stabilizing agent nedocromil sodium, the anticholinergic agent ipratropium bromide, and the H1 receptor antagonist levocabastine are being investigated for intranasal use in the management of allergic rhinitis.
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PMID:Management of allergic rhinitis: focus on intranasal agents. 257 39

Parasympathetic innervation of the respiratory tract of nasal mucosa plays an important role in the pathogenesis of chronic hypertrophic non-allergic rhinitis (C.H.N.A.R.), the vidian nerve providing the main parasympathetic nerve supply to respiratory mucosa. The present study investigates the effect of vidian nerve resection in 22 patient with intractable C.H.N.A.R. on histamine content and formation and on the number of mast cells and their degranulation in the respiratory tract. Samples were taken from respiratory mucosa for histamine and histidine-decarboxylase assay, and for microscopic observations for mast cell density and degranulation index, before and 12-24 months after vidian nerve resection. Neurectomy of the vidian nerve completely cured the clinical symptomatology, evaluated by rhinoreomanometry, and also significantly decreased both the high histamine levels and histidine-decarboxylase activity in patients with C.H.N.A.R. The density and degranulation index of mast cells were also significantly lower after surgery. These data suggest a relationship between cholinergic activity and the secretory response of mast cells and indicates a correlation between the parasympathetic nerve supply and chronic hyperthrophic non-allergic rhinitis. The significant reduction in mast cell density, histamine levels and histidine-decarboxylase activity also lends support to the hypothesis that the parasympathetic nerve supply plays a role in the regulation of mast cell histamine.
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PMID:Vidian nerve resection, histamine turnover and mucosal mast cell function in patients with chronic hypertrophic non-allergic rhinitis. 259 75

With some exceptions, the late asthmatic response and increased airway responsiveness to methacholine or histamine are closely associated. Increased responsiveness after an allergen challenge can be reversed or prevented by appropriate anti-inflammatory treatment. To determine how the inflammatory response contributes to an increase in smooth muscle responsiveness in asthma, local hematopoietic processes were examined. In support of the mast cell hypothesis, scrapings from nasal turbinate mucosa have shown greater numbers of mast cells in patients with allergic rhinitis compared with normal subjects. Similarly, the number of metachromatic cells in bronchoalveolar lavage fluid correlates directly with methacholine-induced airway hyperresponsiveness. Since nasal polyps appear to result from inflammation of nasal mucosa, these tissues were also examined for the possible presence of progenitor cells that favor selective growth of basophil/mast cells. Since growth factors such as interleukins and cytokines stimulate cell activation, they may also contribute to ongoing inflammatory processes. Therefore substances that modify the production or actions of locally generated growth factors might be developed for the treatment of chronic inflammation of the nasal and bronchial airways.
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PMID:Late-phase airway reaction and inflammation. 264 48

Since both allergic asthma and allergic rhinitis are inflammatory respiratory responses, study of a nasal challenge model should help elucidate mediator release in the allergic diathesis of the lower airway. Total allergen load and "priming" are significant factors in nasal and bronchial reactivity. In IgE-mediated allergic reactions, an immediate early response is followed by a delayed response, with symptoms persisting after exposure to allergen. With immunotherapy, IgG titers rise, and the clinical response reflects a balance between the protective IgG response and the IgE-mediated allergic response. In the model studied, mast cell activation and mediator release correlated with the onset of early-phase allergic symptoms. By reducing the magnitude of mediator release and the severity of symptoms, immunotherapy may be used along with environmental controls and pharmacologic therapy to "turn off" the allergic reaction.
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PMID:Immunotherapy in asthma. 264 52

N-Acetyl-aspartyl magnesium glutamate (Rhinaaxia, NAAGA) is a new antiallergic substance for topical use. The compound covers a bilateral way of action. There is inhibition of the mast cell-degranulation and blocking of the C3-convertase, subsequently followed by a blocked cleavage of the fragments C3a and C5a, respectively. 20 patients suffering from perennial allergic rhinitis were treated according to a randomized double blind placebo-controlled study design. Apart from a nominal documentation of subjective complaints the degree of nasal obstruction was objectively rated via rhinomanometria. The nasal flow rate improved significantly in patients treated with NAAGA and subjective complaints decreased markedly. NAAGA showed to be well tolerated although 6 of 10 patients observed transient "nasal burning".
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PMID:[Effectiveness and tolerance of the C3 convertase inhibitor, N-acetyl-aspartyl-magnesium glutamate in perennial rhinitis. Results of a double-blind, placebo-controlled study]. 265 3


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