Coleman Laura, Laing Ingrid A, Bosco Anthony
aTelethon Kids Institute, West Perth bSchool of Paediatrics and Child Health, University of Western Australia, Perth, Western Australia, Australia.
Curr Opin Allergy Clin Immunol. 2016 Apr;16(2):179-85. doi: 10.1097/ACI.0000000000000245.
This article discusses recent findings into the mechanisms that determine how viruses trigger asthma exacerbations.
Substantial progress has been made in our understanding of the pathogenesis of virus-induced asthma exacerbations. This includes new insights into the role of bacteria, the regulation of interferon responses, and the discovery of innate immune pathways that link viral infections with allergic inflammation. Progress has also been made in elucidating the genetic risk factors for asthma exacerbations, most notably the contribution of the ORMDL3/GSDMB locus on 17q, the mechanisms underlying the farming effect, and the discovery that CDHR3 binds to rhinovirus species C.
Asthma exacerbations are heterogeneous conditions that involve the complex interplay between environmental exposures and innate and adaptive immune function in genetically predisposed individuals. Recent insights into the interrelationships between these factors provide new opportunities for therapeutic intervention.
本文讨论了关于病毒引发哮喘加重机制的最新研究发现。
我们对病毒诱发哮喘加重的发病机制的理解取得了重大进展。这包括对细菌作用的新见解、干扰素反应的调节，以及发现了将病毒感染与过敏性炎症联系起来的固有免疫途径。在阐明哮喘加重的遗传风险因素方面也取得了进展，最显著的是17号染色体上ORMDL3/GSDMB基因座的作用、农耕效应的潜在机制，以及发现CDHR3与鼻病毒C型结合。
哮喘加重是一种异质性病症，涉及环境暴露与遗传易感性个体的固有免疫和适应性免疫功能之间的复杂相互作用。对这些因素之间相互关系的最新见解为治疗干预提供了新机会。
