作者: Behzad Yeganeh , Connie Xia , Hesam Movassagh , Cynthia Koziol-White , Ying Chang
DOI: 10.1016/J.PUPT.2012.06.011
关键词: Asthma 、 Pathophysiology 、 Airway smooth muscle 、 Inflammation 、 Semaphorin 、 Bronchial hyperresponsiveness 、 Medicine 、 Immunology 、 Airway Wall Remodelling 、 Phenotype
摘要: Abstract Phenotypic changes in airway smooth muscle are integral to the pathophysiological that constitute asthma – namely inflammation, wall remodelling and bronchial hyperresponsiveness. In vitro in vivo studies have shown proliferative, secretory contractile functions of dysfunctional asthma. These can be modulated by various mediators whose levels altered asthma, derived from inflammatory cells or produced itself. In this review, we describe emerging roles CXC chemokines (GROs, IP-10), Th17-derived cytokines (IL-17, IL-22) semaphorins, as well influence viral infection on function, with a view identifying new opportunities for therapeutic intervention