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)

We have demonstrated that kinins are generated following nasal challenge with allergen of allergic (5.6 +/- 0.17 ng/m-), but not nonallergic (0.04 +/- .02 ng/ml), individuals (n = 8 in each case). The presence of kinin was highly correlated with that of histamine and TAME-esterase activity and with clinical symptoms (p less than 0.001). In a double blind, placebo-controlled study, topical administration of the drug Azatadine, which inhibits mast cell mediator release in vitro, reduced the clinical response to allergen challenge and reduced the concentrations of kinins, histamine, and TAME-esterase activity observed following allergen challenge. In addition to the immediate response to allergen, some individuals experience a recurrence of symptoms some 3-12 hours after challenge; in seven such individuals (13.5 +/- 3.2 ng kinin/ml in the immediate reaction), there was a second increase in nasal kinins (2.95 +/- 1.4 ng/ml) during this late reaction, again correlating with increases in histamine and TAME-esterase activity. HPLC analysis revealed that a mixture of bradykinin and lysylbradykinin is produced during both responses. Finally, 12 subjects with a history of nasal symptoms upon exposure to cold, dry air (CDA) were compared to five asymptomatic individuals in a nasal challenge system involving nasal breathing of CDA and warm, moist air (WMA). For the symptomatic group the levels of kinin in nasal lavages were significantly increased after CDA (2.9 +/- 0.8 ng/ml) compared to baseline (0.06 +/- 0.01 ng/ml) or WMA (0.3 +/- 0.07 ng/ml). Kinin generation again correlated with increases in histamine, PGD2 and TAME-esterase activity and with onset of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinins as mediators of human allergic reactions. 381

A novel human in vivo model of intranasal challenge with antigen is used to demonstrate the effectiveness of a topical antirelease drug. Previous experimentation has established a highly significant correlation between the physiologic response of sneezing, which occurs after insufflation of antigen into the nose of allergic individuals, and the recovery of putative mast cell mediators: histamine, tosyl arginine methyl ester (TAME)-esterase(s), and prostaglandin D2- Azatadine base, a tricyclic antihistamine, which also inhibits mediator release in vitro, applied prior to antigen administration not only reduces the clinical symptom of sneezing but simultaneously reduces the concentration of the inflammatory mediator, TAME-esterase(s), recovered from nasal washes. To our knowledge, this is the first observation that an antirelease drug can stop mediator release in vivo in the nose.
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PMID:In vivo model for the evaluation of topical antiallergic medications. 613 98