ANTI-IGE RESPONSE IN HUMAN AIRWAYS - RELATIVE CONTRIBUTION OF INFLAMMATORY MEDIATORS

HUMAN airway preparations at resting tone were relaxed with either the leukotriene synthesis inhibitor BAY x1005 (3 mu M), chlorpheniramine (1 mu M) or the thromboxane receptor antagonist BAY u3405 (0.1 mu M). The response to anti-IgE (1:1000) was 58 +/- 8% of acetylcholine preco ntraction (2.19 +/- 0.28 g). Indomethacin (3 mu M) enhanced the anti-I gE-induced contraction by 28%. The anti-IgE maximal response was not m odified by either chlorpheniramine, BAY x1005 or BAY u3405. When the t issues were treated with either BAY x1005/indomethacin or BAY x1005/ch lorpheniramine, the anti-IgE-induced contraction was reduced in additi on, in presence of BAY x1005/indomethacin/chlorpheniramine the respons e was completely blocked. These results suggest that mediators release d during anti-IgE challenge cause airway contraction which may mask th e evaluation of the leukotriene component.