Anti-IgE Response in Human Airways: Relative Contribution of Inflammatory Mediators
Heman airway preparations at resting tone were relaxed with either the leukotriene synthesis inhibitor BAY x1005 (3 μM), chlorpheniramine (1 μM) or the thromboxane receptor antagonist BAY u3405 (0.1 μM). The response to anti-IgE (1:1000) was 58 ± 8% of acetylcholine pre-contraction (2.19 ± 0.28 g)....
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
1994-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/S0962935194000505 |
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| Summary: | Heman airway preparations at resting tone were relaxed with either
the leukotriene synthesis inhibitor BAY x1005 (3 μM),
chlorpheniramine (1 μM) or the thromboxane receptor antagonist
BAY 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-induced
contraction by 28%. The anti-IgE maximal response was not
modified by either chlorpheniramine, BAY x1005 or BAY u3405. When
the tissues were treated with either BAY xl005/indomethacin or
BAY x1005/chlorpheniramine, the anti-IgE-induced contraction was
reduced. In addition, in presence of BAY
xl005/indomethacin/chlorpheniramine the response was
completely blocked. These results suggest that mediatots released
during anti-IgE challenge cause airway contraction which may mask
the evaluation of the leukotriene component. |
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| ISSN: | 0962-9351 1466-1861 |