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Neutrophil–induced human bronchial hyper responsiveness in vitro —pharmacological modulation
Author(s) -
HUGHES J. M.,
McKAY K. O.,
JOHNSON P. R.,
TRAGOULIAS S.,
BLACK J. L.,
ARMOUR C. L.
Publication year - 1993
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.1993.tb00318.x
Subject(s) - in vitro , modulation (music) , immunology , medicine , biology , philosophy , biochemistry , aesthetics
Summary Although it has been postulated that inflammatory cells cause the bronchial hyper‐responsiveness which is diagnostic of asthma [1], until recently there has been little direct evidence of such a link. We have recently shown that calcium ionophore‐activated human neutrophils and eosinophils can induce a state of human airway hyperresponsiveness in vitro [2]. In this study we have shown that the anti‐inflammatory agent nedocromil sodium, 10 ‐7 m , inhibited the hyperresponsiveness induced by products released from ionophore activated neutrophils but did not inhibit the release of leukotriene B 4 from the same cells. Neutrophil‐induced bronchial hyperresponsiveness was also inhibited by pre‐treatment of the bronchial tissues with a thromboxane A 2 and prostaglandin receptor antagonist, GR32191,10 ‐7 m . These findings indicate that cyclooxygenase products are involved in bronchial hyperresponsiveness induced by inflammatory cell products in vitro and that their release can be inhibited by nedocromil sodium.