Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/23463
Title: Airway smooth muscle modulation and airway hyper-responsiveness in asthma: new cellular and molecular paradigms.
Authors: Amrani, Y
First Published: May-2006
Citation: EXPERT REV CLIN IMMUNOL, 2006, 2 (3), pp. 353-364
Abstract: There is growing evidence indicating the existence of a causal relationship between abnormal airway smooth muscle (ASM) function and airway hyper-responsiveness, a poorly understood feature of asthma that can be defined as an excessive bronchospastic response. In recent years, there has been a veritable explosion of articles suggesting that ASM exposed to proasthmatic cytokines can elicit a hyper-responsive state to contractile G-protein-coupled receptor (GPCR) agonists. Aberrant airway responsiveness could result from abnormal calcium signaling, with changes occurring at various levels of GPCR-associated signal transduction. This review presents the latest observations describing novel mechanistic models that could explain the involvement of ASM in airway hyper-responsiveness. This review will discuss the role of ASM in beta(2)-agonist-mediated bronchial hyper-responsiveness and the clinical significance of cell-cell contact between ASM and mast cells recently described to be intimately infiltrated within the ASM tissues in asthmatic patients. The possibility that allergens could trigger airway hyper-responsiveness by directly acting on ASM via activation of immunoglobulin E receptors, FcepsilonRI and FCepsilonRII will also be discussed. These important findings further support the notion that targeting ASM could offer new treatment for many features of asthma, including airway hyper-responsiveness. Future therapeutic intervention includes: the prevention of ASM-inflammatory cell physical and/or functional interaction, the inhibition of Immunoglobulin E receptor-dependent signal transduction, and the abrogation of cytokine-dependent pathways that modulate receptor-associated calcium metabolism.
DOI Link: 10.1586/1744666X.2.3.353
eISSN: 1744-8409
Links: http://hdl.handle.net/2381/23463
Type: Journal Article
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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