作者: Yves Landry , Jean-Pierre Gies , Didier Scherrer , Fabien Schmidlin , Laurent Daeffler
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摘要: We investigated the hypothesis that inflammatory mediators such as interleukin-1beta (IL-1beta) might be responsible for hyperreactivity of asthmatic patients to bradykinin. In cultured human bronchial smooth muscle cells, IL-1beta elicited a rapid and transient increase in density bradykinin B2 receptors without affecting their affinity ligands. The was correlated an enhancement inositol phosphate formation by bradykinin, indicating its relevance contractile response cells receptor related mRNA level corresponding 5-fold transcriptional rate lengthened half-life mRNA. These effects were largely inhibited indomethacin, suggesting involvement prostanoid pathway transduction process. An prostaglandin E2 levels preceded increase, confirming this involvement. Moreover, led cAMP formation. propose predominant stimulate transcription gene major mechanism involved hyperresponsiveness