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 total of 61 middle ear effusions and matched sera obtained from patients suffering from chronic otitis media with effusions (OME) was examined for IgE and other immunoglobulins to see if a reaginic antibody is involved in OME. The IgE levels were determined by the Phadebas IgE radioimmunoassay test. Excluding one patient who had extremely high IgE as a result of parasitosis, there were only three cases which showed marginally increased serum IgE levels. Elevated IgE levels in sera and/or in effusions were unrelated to a history of allergy. The mucoid effusions had significantly higher effusion levels than the levels in corresponding sera (p less than .0005). Fourteen percent of the cases examined showed effusion IgE levels five times or more higher than serum levels. Biopsy specimens of these patients showed numerous degranulating mast cells. Only two specimens showed eosinophilic infiltration. It is suggested that the IgE is produced locally by the mucosa in mucoid-type effusions and may have been involved in mast cell degranulation. However, this study cannot confirm the allergic nature of the OME.
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PMID:Immunoglobulin E in chronic middle ear effusions. 126 36

The mast cell--an important component of connective tissue--carries in its cytoplasmic granules various biologically active substances, such as heparin, histamine, and a broad spectrum of enzymes. This cell type plays a prominent role in inflammatory and allergic conditions. In the middle ear, the mast cells are mainly localized in the pars flaccida of the tympanic membrane and beneath the tracts of secretory and ciliated cells in the middle ear mucosa. Degranulation of the mast cells by the histamine liberator compound 48/80 causes histamine-rich effusion material to accumulate in the middle ear. Plugging of the eustachian tube and/or tympanic isthmus will bring about a similar accumulation. It would thus seem that mast cells in some way participate in the production of middle ear effusion, probably via their potent mediators.
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PMID:Mast cells and middle ear effusion. 240 31

Twenty-two surgical specimens of eroded middle ear ossicles were removed from patients with chronic otitis media, with and without cholesteatoma. By using specific mast cell stains, increased numbers of mast cells were found in connective or granulation tissue adjacent to eroded surface of the bone. Mast cells possess the biological machinery necessary for enhancing bone resorption, and the population density of mast cells is increased in a variety of disorders that are associated with bone resorption. It is hypothesized that mast cells contribute to bone resorption in chronic otitis media, and the possible mechanisms by which mast cells exert their action are discussed.
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PMID:Bone resorption in chronic otitis media. The role of mast cells. 241 Nov 2

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

The distribution of mast cells was studied in normal human middle ear mucoperiosteal lining and in middle ear biopsies of patients with acute and chronic otitis media. The mast cells were identified on the basis of the metachromatic staining for their cytoplasmic granules with Giemsa and toluidine blue. Only a few mast cells located in proximity to blood vessels in the lamina propria underneath the epithelial layer were observed in normal middle ear mucoperiosteum. The number of mast cells in acute inflammatory reactions and in the normal middle ear lining was similar. By contrast, the mast cell count was significantly increased in chronic inflammatory reactions. The population density of the mast cells was the highest in the subepithelial layer of cholesteatoma, in regions where the lamina propria showed fibrosis and infiltration with chronic inflammatory cells, and around mucous glands. The presence of increased numbers of mast cells in chronic otitis media is consistent with our previous finding of high levels of histamine in middle ear effusions. It is postulated that mast cells play an important role in the pathogenesis of chronic otitis media through the release of their active biochemical mediators.
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PMID:Mast cells in human middle ear mucosa in health and in disease. 608 6

In this experimental study performed on the rat middle ear either the Eustachian tube or the tympanic isthmus was blocked via the tympanic bulla with a polyethylene plug or a piece of Gelfoam, respectively. Effusion material was immediately observed in the attic space and subsequently the pars flaccida was drawn in a medial direction to form a retraction pocket. The initial changes in the pars flaccida structure were a degranulation of the mast cells and concomitantly metaplasia of the mucosal epithelium into cells displaying numerous osmiophilic inclusions, vacuoles and multivesicular bodies. It cannot be excluded that the initial cause of the effusion production is the histamine released from mast cell granules.
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PMID:Structure of the pars flaccida after occlusion of the Eustachian tube or blockade of the tympanic isthmus. 711 52

The distribution of mast cells in the adenoidectomy specimens of 76 children with enlarged adenoids was studied. Forty of the patients had secretory otitis media; the remaining 36 had normally aerated middle ears. The mast cells were identified on the basis of the metachromatic staining of their cytoplasmic granules with toluidine blue. Patients with secretory otitis media had a twofold increase of their mast cell population compared to those without middle ear disease. Statistical analysis confirmed that the difference between the two groups is significant (p = .0001). The results of the study are consistent with the previous finding of increased histamine concentration in adenoids of children with secretory otitis media and lend support to the adenoid mediator release hypothesis, whereby the adenoid mast cells degranulate and release histamine and other inflammatory mediators that induce eustachian tube insufficiency and otitis media with effusion.
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PMID:Possible role of adenoid mast cells in the pathogenesis of secretory otitis media. 806 58

The mast-cell-specific proteolytic enzymes tryptase and chymase were identified in and isolated from cholesteatoma in a ratio similar to that found in human skin. We assume that this ratio reflects a similar distribution of tryptase-containing and tryptase/chymase-containing mast cells in both these tissues. It seems conceivable that mechanisms able to trigger excessive and/or continuous mast cell degranulation in the middle ear might be causative for the formation of cholesteatoma either directly or via primed chronic inflammatory reactions. By their ability to amplify degranulation of mast cells, mast cell proteinases, in particular chymase, may contribute to the chain of events leading to the formation of cholesteatoma.
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PMID:Isolation and characterization of trypsin-like and chymotrypsin-like proteinases from human cholesteatoma. 817 64

Mast cells are known to reside in pars flaccida membranae tympani and other parts of the middle ear mucosa in both rats and humans. However, the normal pars tensa contains no or only a few mast cells along the manubrial vessels. We examined the pars tensa of 25 rats in an experimental model of acute otitis media and found 13 mast cell clusters in 6 membranes. A majority of clusters were located in the anterior, superior quadrant and contained from 3 to 23 cells. The mast cells resided immediately under the inner epithelial lining or in the intermediate, fibrous layer. In two membranes mast cell clusters were found in the margin of apparently healed spontaneous perforations. We conclude that mast cells in some cases infiltrate pars tensa membranae tympani in the late and receding phase of acute otitis media. As these cell clusters in some cases were found immediately around apparently healed membrane perforations, we propose that the mast cell might participate in the repair processes of tympanic membrane perforation healing. This is supported by recent studies in wound healing and functions of a number of mast cell mediators.
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PMID:Mast cell clusters in pars tensa membranae tympani in acute otitis media: a possible role in perforation healing. 897 19

The inhibitory effects of ketotifen, a histamine H1-receptor antagonist and mast cell stabilizer, were examined on a non-IgE experimental model of middle ear effusion. Thirty rats were divided into three groups. Group A (n = 9) was subjected to mechanical stimulation of the external auditory canal (EAC); group B (n = 11) was pre-treated with intraperitoneal administration of 0.2 mg ketotifen, 90 min before mechanical stimulation of the EAC; and group C (n = 10), the control group, was neither exposed to mechanical stimulation nor given ketotifen. Thirty minutes after completion of the experiment, the eardrums were inspected, histamine levels were determined by a fluorometric assay, and the pars flaccida underwent histological assessment. An attic effusion was observed in group A; a similar phenomenon but to a lesser extent was also seen in group B. Statistical analysis confirmed that the mean histamine concentration of the rinsing fluid obtained from group A was significantly higher than that of group C (p = 0.004) or group B (p = 0.008). No significant difference was found between the mean histamine concentration of groups C and group B (p = 0.311). Histological assessment revealed that the thickness of the pars flaccida of group A was considerably greater than that of groups C and B and was characterized by marked edema. Furthermore, the pars flaccida mast cell population was significantly depleted compared with groups C and B. The data indicate that mechanical stimulation of the EAC triggered the pars flaccida mast cells to degranulate in a non-mediated IgE fashion and that histamine is implicated in most of these histological changes. It is concluded that administration of ketotifen before mechanical stimulation of the EAC had a stabilizing effect and abolished mast cell degranulation, therefore, may be considered as a potential therapeutic agent for the treatment of middle ear disease in the pediatric population.
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PMID:Ketotifen induced inhibition of histamine release in a non-IgE model of middle ear effusion. 1642 54


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