Anti-IgE Response in Human Airways: Relative Contribution of Inflammatory Mediators

[摘要] Heman airway preparations at resting tone were relaxed with eitherthe leukotriene synthesis inhibitor BAY x1005 (3 μM),chlorpheniramine (1 μM) or the thromboxane receptor antagonistBAY u3405 (0.1 μM). The response to anti-IgE (1:1000) was 58± 8% of acetylcholine pre-contraction (2.19 ±0.28 g). Indomethacin (3 μM) enhanced the anti-IgE-inducedcontraction by 28%. The anti-IgE maximal response was notmodified by either chlorpheniramine, BAY x1005 or BAY u3405. Whenthe tissues were treated with either BAY xl005/indomethacin orBAY x1005/chlorpheniramine, the anti-IgE-induced contraction wasreduced. In addition, in presence of BAYxl005/indomethacin/chlorpheniramine the response wascompletely blocked. These results suggest that mediatots releasedduring anti-IgE challenge cause airway contraction which may maskthe evaluation of the leukotriene component.

[学科分类] 生理学与病理学