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)

To examine mast cell involvement in allergic rhinitis, levels of tryptase, a specific marker for mast cell activation, and histamine, a marker of mast cell and basophil activation, were measured in nasal-lavage fluid after nasal-allergen challenge. Twelve atopic subjects with allergic rhinitis and five nonatopic subjects were challenged with timothy grass or ragweed pollen at increasing doses of allergen. Tryptase and histamine levels were determined by an ELISA and radioenzyme assay, respectively; clinical responses were measured by assessment of sneezing, rhinorrhea, nasal congestion, and ocular tearing or itching. A positive clinical response was observed in seven of the atopic subjects and in none of the nonatopic subjects. Tryptase levels increased at least sevenfold higher than baseline levels in 100% of the atopic clinical responders and reached a maximum at the same dose of allergen where clinical symptoms were maximal. In contrast, histamine levels were only threefold or greater elevated in five of seven atopic clinical responders at this dose of allergen. (Histamine levels were lower in one subject and were only 50% higher in another subject than the corresponding baseline value.) Histamine levels and symptom scores were maximal at the same dose of allergen in only four of seven clinical responders. Overlap of peak mediator levels in subjects without a clinical response with those of the clinical responders occurred only in the case of histamine. Tryptase levels in nasal-lavage fluid appear promising as a useful indicator of allergic reactions and indicate that mast cell activation is the major factor in the immediate nasal-allergic response.
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PMID:Tryptase levels in nasal-lavage fluid as an indicator of the immediate allergic response. 304 43

Allergic antibodies, now known to be of the IgE class, have been associated with basophil and mast cell activation and thus with histamine release since these cells contain histamine. Common allergen induced diseases such as allergic rhinitis have been correlated with IgE antibody, basophils, mast cells and histamine release and partial control with pharmacologic use of histamine receptor blockade. This report now classifies all immediate-type reactions in reference to basophils and mast cells and activation of these cells. This approach appears particularly important in relation to those immediate-type reactions which simulate IgE mediated responses but in which no allergenic stimulus is present. The mechanisms of pharmacologic control of these basophil-mast cell response syndromes and potential research approaches are emphasized.
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PMID:Basophil-mast cell response syndromes: a unified clinical approach. 306 89

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

The role of IgE-mediated hypersensitivity in the development of middle ear disease has not been completely resolved. However, on the basis of our investigations and those of other laboratories, we suggest that approximately two thirds of patients with chronic recurrent otitis media do not have allergies. The other third may have allergic rhinitis, and this allergic rhinitis could play a direct role in producing eustachian tube dysfunction in recurrent otitis media. However, viral infections of the upper respiratory tract may also induce IgE-mediated release of mast cell inflammatory mediators, and could cause otitis media on the basis of viral infection alone. Subtle immunologic deficiencies involving the IgG2 subclass and other immunoglobulin subclasses may also be lower in otitis-prone children, and this may be a genetically inherited disorder. Finally, the possibility of food allergy in otitis media must be considered, particularly in the young otitis-prone child with chronic recurrent otitis media.
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PMID:Recent advances in immunologic reactivity in otitis media with effusion. 328 24

To investigate the pathogenesis of allergic rhinitis, we developed a nasal challenge model in which we examined the early, late, and rechallenge responses to antigen provocation. In these three aspects of the allergic reaction the physiologic responses are associated with inflammatory mediator release. Whereas the early response appears to be related mainly to mast cell activation and mediator release, the late reaction involves a different pattern of mediator release and an inflammatory cell influx, consisting of basophils, neutrophils, and eosinophils. Rechallenge with antigen 11 hours later results in an augmented immediate response. Pretreatment with aspirin reduces the levels of cyclooxygenase metabolites in nasal secretions without affecting the immediate physiologic response to antigen or the expected increase in the levels of histamine, N-alpha-tosyl-L-arginine methyl ester-esterase activity, and leukotriene C4. Pretreatment with systemic steroids does not affect the early allergic response, but significantly reduces mediator release during the late and rechallenge responses. The influx of eosinophils is inhibited by pretreatment with systemic steroids, but neutrophil influx is not. In contrast, pretreatment with topical steroids blocks the early response and the late and rechallenge responses. Influx of all cell types, including the neutrophil, was prevented. These studies show unequivocally that an inflammatory process follows the initial response to antigen and that this inflammation is affected by drugs important in the treatment of chronic allergic disease. We speculate that understanding allergic inflammation will lead to new therapeutic development.
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PMID:Experimentally induced nasal allergic responses. 337 15

The ultrastructure of mast cells found in normal inferior turbinate was compared with the features found in the inferior turbinate in two groups of patients, those with allergic rhinitis due to dust mite hypersensitivity and those with nasal polyps; the latter group also had their polyps studied. Adenoid tissue was examined in children with secretory otitis media to see if there was evidence of mast cell degranulation, which would support the hypothesis that either local allergic or other mast cell-mediated reactions caused the condition. The mast cells from five normal turbinates varied considerably in size, shape and distribution, but were found mainly in the submucosa. There was no difference in the morphology of cells of different sizes and they could not be sub-grouped into either connective tissue or mucosal mast cells. Most granules were electron dense and homogeneous, although scrolls and crystalline structures were seen occasionally. Some of the granules contained lighter material and others had become vacuoles. Mitochondria were present in all cells suggesting active metabolism. The three patients with allergic rhinitis showed extensive but variable degranulation of the mast cells in all depths of the mucosa. Nine of the 10 cases with nasal polyps had mast cells identified in both the polyp and the turbinate. They were only normal in one turbinate and in one patient it was impossible to identify mast cells. All the mast cells were degranulated extensively in all other specimens. The adenoids from seven children had identifiable mast cells, which were less frequently found than in the turbinates. There was some degranulation in four of the patients and in one it was fairly extensive.
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PMID:Nasal mast cells: a preliminary report on their ultrastructure. 348 65

Light- and electronmicroscopic observations as well as immunohistochemical studies were made on nasal polyps from 15 patients. The patients included 2 cases of aspirin intolerance (AA), 6 cases of allergic rhinitis (NA) and 7 cases of chronic rhinitis (CS) with negative skin tests against major inhalant allergens. Nasal polyps commonly contained many inflammatory cells such as neutrophils (PMN), eosinophils, plasma cells, mast cells, lymphocytes and macrophages. Two morphological features were conspicuous in our study: 1) PMN migration and attachment to the basal lamina, 2) accelerated degranulation of mast cells. Mean values of degranulated granules were 0.532473/micron2 in AA, 0.492615/micron2 in NA and 0.253591/micron2 in CS. These results indicate that mast cell degranulation in CS is much less than that in AA and NA. Immunohistochemical investigations revealed very few IgE-positive cells in both AA and NA, and none in CS. On the other hand IgG and IgA were frequently observed in all cases of nasal polyps. The present study suggests that mast cell degranulation plays an important role in the formation of nasal polyps, but it may not only be an IgE-dependent mechanism. To elucidate other possibilities, more extensive immunological studies will be required.
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PMID:Mast cell degranulation in nasal polyps. 352 8

The mechanisms underlying allergic tissue basophil/mast cell (BMC) or eosinophil (Eo) accumulation are unclear, especially since chemotaxis or IgE levels do not offer a sufficient explanation. We have found that a formaldehyde-blockable, steroid-responsive nasal metachromatic cell (NMC) population predominates in epithelium and correlates well with symptoms and signs in patients with allergic rhinitis. Circulating BMC and Eo progenitors (colony-forming cells in culture; CFU-c) are increased in atopic patients, inversely related to NMC counts, and fall as NMC numbers rise during seasonal allergen (ragweed pollen) stimulation. The metachromatic cell progeny of these CFU-c are also formaldehyde-blockable in their staining reaction and thus may correspond to NMC. Human nasal polyps yield BMC CFU-c. Nasal polyp epithelial scrapings or mononuclear cells, T lymphocytes or keratinocytes in vitro all produce potent BMC or Eo colony-stimulating activities (CSA) as well as an interleukin-3-like activity, each of which is partially separable from the others. Nasal epithelial cells cultured from scrapings of atopic, as opposed to nonatopic, patients also produce BMC or Eo CSA with an enhanced effect of the former on atopic peripheral blood CFU-c growth. These studies support the hypothesis that BMC and Eo accumulate in allergic inflammation as a result of in situ growth and differentiation of progenitors stimulated by soluble hemopoietic factors derived from mucosal cell populations.
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PMID:Contribution of basophil/mast cell and eosinophil growth and differentiation to the allergic tissue inflammatory response. 355 23

Symptomatic seasonal allergic rhinitis has previously been found to be associated with a redistribution of mast cells from the subepithelial stroma to the epithelial lining and the surface of the nasal mucosa. The present study was designed in order to elucidate the interaction between topical glucocorticosteroids, effective in the treatment of allergic rhinitis, and the migration of mast cells described earlier. Six patients treated prophylactically in the nose with budesonide were studied. Imprints and biopsies from the nasal mucosa were taken 2-3 weeks before and 2-3 weeks into the birch pollen season. The biopsies were used for light microscopy and tissue histamine determination. The morphologic studies showed, also in the actively treated patients, an increased number of metachromatically stained cells on the nasal mucosal surface of the same order of magnitude as previously reported for untreated patients. We did, however, find a decrease in the histamine content of the nasal mucosa, which was not associated with a decrease in the number of mast cells. Together with similar previous findings in the unstimulated allergic nasal mucosa these results suggest that glucocorticosteroids induce a decrease in the mast cell histamine pool, possibly due to an inhibition of the intracellular synthesis of histamine. This effect might contribute to the clinically beneficial effect of topical glucocorticosteroids in the treatment of hay fever.
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PMID:Nasal mucosal mast cells and histamine in hay fever. Effect of topical glucocorticoid treatment. 365 99

We employed bronchoalveolar lavage (BAL) of subsegmental airways to study the local inflammatory effects of aeroallergen bronchoprovocation (BPC) and local instillation of allergen in allergic asthmatic patients, allergic rhinitis patients, and normal subjects. Two protocols were used: (1) BAL was performed in three subsegments following BPC or during spontaneous seasonal exposure, and (2) 5-ml aliquots of increasing doses of allergen were instilled into a single subsegment until there was at least 30 percent closure of the airway; the airway was then immediately lavaged. A subsegment in the opposite lung was lavaged as a control site. These same two segments were lavaged again two to 14 days later and the cells and fluid analyzed. Fifty-five lavages have been performed without complications. Pulmonary function tests (FEV1) were not significantly disturbed by either local challenge or lavage procedures. Cells were examined using light and electron microscopy and showed inflammatory cells in alveolar airways and dissolution of mast cell and eosinophil granules. Using selected criteria, we were able to use these methods in mildly, seasonally asthmatic patients to obtain safely cells and fluid for analysis. These techniques may permit studies which further our understanding of the mechanisms responsible for allergic asthma.
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PMID:Methods for bronchoalveolar lavage in asthmatic patients following bronchoprovocation and local antigen challenge. 396 37


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