title: Emerging mediators of airway smooth muscle dysfunction in asthma.
abstract: Phenotypic changes in airway smooth muscle are integral to the pathophysiological changes that constitute asthma - namely inflammation, airway wall remodelling and bronchial hyperresponsiveness. In vitro and in vivo studies have shown that the proliferative, secretory and contractile functions of airway smooth muscle are dysfunctional in asthma. These functions can be modulated by various mediators whose levels are altered in asthma, derived from inflammatory cells or produced by airway smooth muscle itself. In this review, we describe the emerging roles of the CXC chemokines (GROs, IP-10), Th17-derived cytokines (IL-17, IL-22) and semaphorins, as well as the influence of viral infection on airway smooth muscle function, with a view to identifying new opportunities for therapeutic intervention in asthma.
authors: Department of Physiology, Manitoba Institute of Child Health, University of Manitoba, Winnipeg, Manitoba, Canada.
authors: Behzad
authors: B
authors: Yeganeh
authors: Connie
authors: C
authors: Xia
authors: Hesam
authors: H
authors: Movassagh
authors: Cynthia
authors: C
authors: Koziol-White
authors: Ying
authors: Y
authors: Chang
authors: Laila
authors: L
authors: Al-Alwan
authors: Jane E
authors: JE
authors: Bourke
authors: Brian G G
authors: BG
authors: Oliver
mesh_terms: D056151:Airway Remodeling; D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity / Q000503:physiopathology; D019743:Chemokines, CXC / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000473:pathology*; D010641:Phenotype; D039961:Semaphorins / Q000378:metabolism
chemical_list: D019743:Chemokines, CXC; D016207:Cytokines; D039961:Semaphorins