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

Mast cells are widely distributed in various organs. Two classes of mast cells, the mucosal mast cell (MMC) and the connective tissue mast cell (CTMC), have been shown to exist in the intestine of experimental animals. In the present study, we investigated the method of staining suitable for observing the mast cells distributing in the nasal mucosa, and also examined by the use of two fixatives whether the mast cells have properties of MMC or those of CTMC. A neutral buffered formalin solution and Carnoy's solution were used as fixative. For staining, five solutions, i.e., toluidine blue (TB) solution (pH 0.5, 2.5, and 4.0), 0.4 M MgCl2-alcian blue (AB) solution, and naphthol AS-D chloracetate (NAS-DC) solution, were tested. In the specimen fixed with Carnoy's fixative, staining with pH 0.5 TB showed the largest number of mast cells in all mucosal layers, particularly in the epithelial layer. The number of these mast cells agreed with that of the cells positive to pH 0.5 AB and also with that of the tryptase-positive cells stained immunohistochemically with a mouse monoclonal antitryptase antibody. Compared with formalin-fixed specimens, those fixed with Carnoy's fixative and stained with pH 0.5 TB showed significantly (p less than 0.01) many mast cells in the epithelial layer and in the subepithelial layer of lamina propria. To identify mast cells in the nasal mucosa with nasal allergy, fixation with Carnoy's fixative and staining with pH 0.5 TB were found to be most effective and simplest.(ABSTRACT TRUNCATED AT 250 WORDS)
Auris Nasus Larynx 1991
PMID:Study on staining methods for mast cells in the nasal mucosa. 172 84

The difference in the non-specific reactivity of lamina propria mast cells in the nasal mucosa of nasal allergy and nonallergic disease was studied. When the nasal mucosa was incubated in three kinds of histamine releasers, the rate of histamine release and that of mast cell degranulation were not statistically different between nasal allergy and nonallergic disease. In the presence of buffer alone, the rate of histamine release did not show the statistical difference between two diseases. However, in the same condition, the degranulation of mast cells in the case of nasal allergy was more than that of nonallergic nasal disease. These results show that the degranulation of mast cells in nasal allergy was more than that in nonallergic nasal disease in the living body. As for non-specific hypersensitivity in the case of nasal allergy, it is considered that one factor is the release of chemical mediators induced by an interaction between allergen and IgE antibodies on the cell membrane of mast cells.
Auris Nasus Larynx 1987
PMID:The reactivity of mast cells in nasal mucosa--comparison between allergic and nonallergic disease. 245 28

Bronchial asthma is a chronic disorder characterized by airway inflammation, reversible airway obstruction, and airway hyperresponsiveness. Eosinophils are believed to play important roles in the pathogenesis of asthma through the release of inflammatory mediators. In refractory eosinophilic asthma, anti-IL-5 mAb reduces exacerbations and steroid dose, indicating roles of eosinophils and IL-5 in the development of severe eosinophilic asthma. Even in the absence of IL-5, it is likely that the "Th2 network", including a cascade of vascular cell adhesion molecule-1/CC chemokines/GM-CSF, can sufficiently maintain eosinophilic infiltration and degranulation. Cysteinyl leukotrienes can also directly provoke eosinophilic infiltration and activation in the airways of asthma. Therefore, various mechanisms would be involved in the eosinophilic airway inflammation of asthma. In the pathogenesis of severe asthma, not only eosinophils but also mast cells or neutrophils play important roles. Mast cells are much infiltrated to smooth muscle in severe asthma and induce airway remodeling by release of inflammatory mediators such as amphiregulin. Treatment with anti-IgE Ab, which neutralizes circulating IgE and suppresses mast cell functions, reduces asthma exacerbations in severe asthmatic patients. Furthermore, infiltration of neutrophils in the airway is also increased in severe asthma. IL-8 plays an important role in the accumulation of neutrophils and is indeed upregulated in severe asthma. In the absence of chemoattractant for eosinophils, neutrophils stimulated by IL-8 augment the trans-basement membrane migration of eosinophils, suggesting that IL-8-stimulated neutrophils could lead eosinophils to accumulate in the airways of asthma. In view of these mechanisms, an effective strategy for controlling asthma, especially severe asthma, should be considered.
Auris Nasus Larynx 2011 Oct
PMID:Pathogenesis of airway inflammation in bronchial asthma. 2133 36