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

In orbital exenteration specimens from 14 rats, 93% of the mast cells were found in the lids, the limbus, and the conjunctiva, 5% in the orbital tissues, and less than 1% in the globe. The density of mast cells was highest in lid (2843/mm3), limbus (2822/mm3), and orbit (2184/mm3) and lowest in bulbar conjunctiva (794/mm3), ciliary body (512/mm3), and sclera (176/mm3). There was no significant difference in the distribution or density of mast cells in orbital exenteration specimens from normal rats compared with rats infected with the worm Nippostrongylus brasiliensis. We concluded that certain ocular structures are rich in mast cells, which suggests that these structures might be susceptible to injury mediated by mast cell products.
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PMID:Mass cells in ocular tissues of normal rats and rats infected with Nippostrongylus brasiliensis. 45 60

A total of thirty pterygia were studied for mast cells using metachromatic dye (toluidine blue) together with routine histological stains. On microscopic examination, the lesion was differentiated and classified into angiomatous, fibrous and mixed varieties based on the vascular and collagenous components. The mast cell counts were undertaken in all types and were found to have significant correlation with the morphological types when compared to normal conjunctiva. 15.1 +/- 3.1, 22.7 +/- 3.8, 9.5 +/- 3.2 mast cell per mm2 were found in the angiomatous, mixed and fibrous types respectively. In the control material, the mast cell count was 12.4 +/- 2.3 per mm2. The results are discussed. It is believed that mast cells are actively involved in the genesis and progress of pterygium.
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PMID:Mast cells and pterygium. 98 51

We studied the effect of one application of compound 48/80 to the conjunctiva of the rat on the response to a subsequent challenge. Rats treated once showed conjunctival edema and marked degranulation of conjunctival mast cells. A second exposure to compound 48/80, applied after an interval of 24 h, produced slight clinical effects but had marked effects on conjunctival mast cells. Approximately 90% of the mast cells could no longer be observed by light microscopy. As the interval between initial challenge and rechallenge was increased, the clinical response returned, mast cells were again observable in normal numbers, and the extent of degranulation returned to approximately 50%. After an interval of 7 days, rats responded clinically as they had to the first application of compound 48/80. Although the number of mast cells in the conjunctiva was normal and extensive degranulation occurred, exocytosis was not observed. Thus some effects of the first application of compound 48/80 persisted for at least 1 week. Whether the effects observed depend upon the continued presence of compound 48/80 in the mast cell or granule membrane remains to be determined.
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PMID:Determination of the interval during which one application of compound 48/80 to the rat conjunctiva influences the response to a second application. 169 8

The presence of eosinophils in the conjunctival epithelium is indicative of allergies, and detection is currently performed by cotton swab scrapings. Although mast cells are thought to be chemotactic for eosinophils and thus presage their accumulation, the former's use as early indicators of allergy has heretofore been hindered by poor detection methods. The recent development of a special brush now makes it possible to collect many cells with less disturbance of the conjunctival epithelium. In the present study, we have used this brush for conjunctival scraping in 18 patients with vernal and allergic conjunctivitis, and 10 patients serving as controls. The superior and inferior tarsal conjunctiva in both eyes were examined, and the specimens were stained using Hansel's method. Mast cells were observed in at least one of the tarsal conjunctivae in all cases of vernal and allergic conjunctivitis, whereas eosinophils were so observed in only eight cases (44.4%). Neither mast cells nor eosinophils were present in the conjunctivae of the normal group. Although treatment by mast cell stabilizers produced clinical remissions, they induced disappearance of mast cells in only 10 cases (55.6%), whereas in six cases (33.3%) the mast cells increased, and in two cases they were unchanged (11.1%). Six cases (33.3%) each showed disappearance of, increase in, and no change in eosinophils, reflecting even less of a response of these allergic cells to the treatment. The presence of mast cells and eosinophils, as determined by our cytologic method, was found to be correlated with the early detection, but not the clinical severity, of allergic conjunctivitis.
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PMID:Detection by brush cytology of mast cells and eosinophils in allergic and vernal conjunctivitis. 178 81

Conjunctival biopsies from 11 patients with atopic keratoconjunctivitis (AKC) and from 13 age-matched healthy individuals undergoing cataract surgery were analyzed by light microscopy and immunohistochemical techniques. Histology of AKC specimens showed goblet cell proliferation, epithelial pseudotubular formation, eosinophil and mast cell invasion of the epithelium, and pronounced mononuclear cell infiltration of the substantia propria, often with frank granuloma formation. Epithelium of AKC conjunctiva showed significantly more T cells (CD3+, CD5+), T-helper cells (CD4+), macrophages (Mac-1+, CD14+), activated T cells, (CD25+), and dendritic cells (CD1+), and a higher helper/suppressor ratio than did control subjects. In the substantia propria, AKC specimens showed dramatically increased inflammatory cell infiltration with significantly more cells staining, in order of frequency, for T-cells (CD3+, CD5+), T-helper cells (CD4+), T-suppressor/cytotoxic cells (CD8+), macrophages (CD14+, Mac-1+) activated T cells (CD25+), B cells (CD22+), and dendritic cells (CD1+, HLA-DR+). Fifty-three percent of T cells in the substantia propria expressed the interleukin-2 receptor protein (CD25+). These findings indicate that the chronic conjunctivitis of AKC is complex, with activated T-cells and macrophages dramatically participating in the process. Successful long-term control of the potentially binding conjunctival inflammation of this disease is likely to require therapeutic strategies directed toward more than just the mast cell component of the process.
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PMID:Immunopathology of atopic keratoconjunctivitis. 192 55

Tryptase, a neutral endoprotease, is secreted by activated mast cells in human tissues. Tryptase levels in various body fluids have been used as an indicator of mast cell activation. The authors determined tryptase levels in unstimulated tears collected from the following groups of patients: (1) normal control, (2) nonallergic ocular inflammation, (3) asymptomatic seasonal allergic conjunctivitis, (4) symptomatic seasonal allergic conjunctivitis, (5) vernal conjunctivitis, and (6) contact lens-associated giant papillary conjunctivitis. They also assessed the release of tryptase into the tear fluid after provoking the conjunctiva with (7) allergens, (8) compound 48/80, and (9) rubbing. Tryptase levels were elevated in tears of patients with active ocular allergy and also increased after provoking the conjunctiva with allergens in atopic subjects and with compound 48/80 and rubbing in nonatopic subjects. Tryptase levels in tear fluid may prove useful as a clinical indicator of mast cell involvement in ocular allergic disorders. In provocation experiments, tryptase levels may be used to evaluate and compare different mast cell stabilizing agents.
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PMID:The level of tryptase in human tears. An indicator of activation of conjunctival mast cells. 208 98

To determine the uniformity of response by mast cells in the rat eyelid, doses of compound 48/80 ranging from 50 to 1,000 micrograms in a 10-microliters drop were applied to one eye of 30 male Sprague-Dawley rats. Phosphate-buffered saline (PBS) was applied to the other eye. Every mast cell was counted throughout microscopic slides of the tissue of the lower eyelids. Both the position and degree of degranulation of every mast cell in each slide were recorded on schematic representations of the lower eyelid. Before histologic examination, animals were observed for clinical signs of ocular anaphylaxis. Doses of 50 and 150 micrograms had no observable clinical effect. At greater doses, edema of the lids and conjunctiva increased with dose. Doses less than 250 micrograms had no significant effect on the number of mast cells or degree of degranulation. Doses of more than 250 micrograms induced degranulation in approximately 50% of the eyelid mast cells. The degree and pattern of degranulation did not change with doses greater than 250 micrograms. The morphology of degranulated mast cells treated with 1,000 or 250 micrograms of compound 48/80 was indistinguishable. We conclude that once maximal stimulation for degranulation is achieved, higher levels of compound 48/80 will not increase the level or change the type of degranulation. In addition, the maximal level of degranulation varies from one mast cell to the next. Mast cells in close proximity may differ markedly in their level of maximal degranulation, with responses ranging from no degranulation to severe degranulation with exocytosis.
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PMID:Morphologic evidence that compound 48/80-challenged rat eyelid mast cells differ in their states of maximal degranulation. 247 97

A single application of the mast cell secretagogue compound 48/80 to the surface of the rat eye induces significant histologic changes. Ocular anaphylaxis is usually the result of repeated, not single, exposures to allergenic substances. The response of conjunctival mast cells to repeated daily applications of compound 48/80 was, therefore, evaluated. Ninety rats received one dose of compound 48/80 or phosphate-buffered saline almost daily for 17 days. The frequency and degree of mast cell degranulation and the number of mast cells and other inflammatory cells in the subepithelial conjunctiva were determined histologically. The clinical response was most marked after one application of compound 48/80; repeated daily applications markedly reduced the clinical response. In eyes treated with multiple applications, 75% fewer mast cells were observable in the conjunctiva by light microscopy compared with phosphate-buffered saline treated eyes. Most mast cells were granulated; a few showed mild to moderate degranulation. Except for epithelial damage, no tissue injury was associated with multiple applications of compound 48/80. In contrast to conjunctivae subjected to a single application of compound 48/80, conjunctivae receiving multiple applications resembled that of phosphate-buffered saline controls.
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PMID:Response of rat conjunctival mast cells to multiple versus single applications of compound 48/80. 248 Dec 51

In the present study we sought to develop a model of ocular anaphylaxis based on the topical application of compound 48/80 to the surface of the rat eye. Doses ranging from 50 to 1000 micrograms were found to produce graded edema of the conjunctiva and swelling of the lid. On histologic examination, 50 microns compound 48/80 produced no changes distinguishable from those in PBS-treated controls, 150 microns produced mild alterations, and 250, 500, and 1000 micrograms compound 48/80 produced a marked increase in degranulated mast cells and a mild influx of neutrophils. The time course of the response to 250 micrograms and 1000 micrograms of compound 48/80 was evaluated over a 72-h period. Both doses elicited epithelial damage. A mild reduction in the number of mast cell was seen at 6 h in rats receiving 250 or 1000 micrograms. The reduction persisted to 72 h in rats receiving 1000 micrograms. The number of neutrophils was increased at 1 and 6 h in eyes treated with 250 micrograms and at 1, 6, and 24 h in eyes treated with 1000 micrograms compound 48/80. The clinical and histologic changes induced by application of 250 micrograms compound 48/80 resemble those seen in patients with allergic conjunctivitis suggesting that a model of ocular anaphylaxis based on the topical application compound 48/80 will be clinically relevant and experimentally practical.
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PMID:Ocular anaphylaxis induced in the rat by topical application of compound 48/80. Dose response and time course study. 255 44

Compound 48/80, a non-immunogenic mast cell degranulatory agent, is known to produce the signs and symptoms of ocular allergy. Maximal mast cell degranulation of human conjunctiva occurred within the first hour after stimulation by a single topical dose of compound 48/80 (20 microliters, 7.5 mg/ml). The average percentage of fully degranulated mast cells in treated specimens (n = 9) was 31% (range 5-60%) versus 6% (range 0-20%) in control specimens (n = 5). Exact correlates of representative granulated, partially degranulated, and fully degranulated mast cells were determined by light and transmission electron microscopy.
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PMID:Time course of human conjunctival mast cell degranulation in response to compound 48/80. 255 45


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