Over-expression of the @entity36092 gene in @entity19 reproduces @entity1 @entity117 -induced XXXX .

@entity10964 @entity25084 @entity32 @entity1 @entity19 @entity565 @entity117 @entity1426 @entity1440 @entity102 @entity223 @entity164 @entity58 @entity36092 @entity6954
BACKGROUND: The pathogenesis of @entity117 -induced @entity565 (AIA) is presumed to involve the @entity117 /non-steroidal anti-inflammatory drug (NSAID)-induced abnormal metabolism of @entity1426 , resulting in an increase in @entity25084 (5-LO) metabolites, particularly @entity223 ( @entity223 ). However, the role of LTC(4) in the development of AIA has yet to be conclusively demonstrated. OBJECTIVE: The aim of this study was to evaluate the contribution of the lipid product LTC(4) secreted by the 5-LO pathway to the pathogenesis of AIA. METHODS: To evaluate antigen-induced @entity32 , the concentrations of T-helper type 2 cytokine in bronchoalveolar lavage fluid (BALF) obtained from @entity36092 -transgenic (Tg) and @entity164 ( @entity164 ) @entity19 after challenge with ovalbumin were measured. Subsequently, the ex vivo and in vivo effects of the NSAID @entity10964 were investigated in these Tg and @entity164 @entity19 by measuring the secretion of LTC(4) from @entity10964 -treated BAL cells and the levels of LTC(4) in BALF following challenge with @entity10964 . Finally, the @entity10964 -induced airway response by the administration of pranlukast, an antagonist of the @entity6954 (cs)-LT1 receptor, was analysed. RESULTS: The concentrations of @entity58 , -5, and -13 in BALF from Tg @entity19 were significantly higher than those in @entity164 @entity19 . In addition, @entity10964 augmented the secretion of LTC(4) in BALF and by BAL cells in Tg @entity19 , but not in @entity164 @entity19 . Additionally, the increased airway resistance induced by @entity10964 could be reduced by treatment with @entity1440 . Furthermore, the secretion of LTC(4) from mast cells, eosinophils, and macrophages was increased in the allergen-stimulated @entity36092 gene Tg @entity19 , even in the absence of @entity10964 , as well as in BAL cells after @entity10964 . CONCLUSION AND CLINICAL RELEVANCE: The over-expression of the @entity36092 in a @entity19 @entity565 model also replicates the key features of AIA. And our study supports that cys-LTs play a major role in the pathogenesis of AIA in @entity1 with @entity102 .
