Kumar Rakesh K, Foster Paul S, Rosenberg Helene F
Department of Pathology, University of New South Wales, Sydney, Australia;
Centre for Asthma and Respiratory Disease, University of Newcastle and Hunter Medical Research Institute, Callaghan, Australia; and.
J Leukoc Biol. 2014 Sep;96(3):391-6. doi: 10.1189/jlb.3RI0314-129R. Epub 2014 Jun 5.
Exacerbations of asthma are most commonly triggered by viral infections, which amplify allergic inflammation. Cytokines released by virus-infected AECs may be important in driving this response. This review focuses on accumulating evidence in support of a role for epithelial cytokines, including IL-33, IL-25, and TSLP, as well as their targets, type 2 innate lymphoid cells (ILC2s), in the pathogenesis of virus-induced asthma exacerbations. Production and release of these cytokines lead to recruitment and activation of ILC2s, which secrete mediators, including IL-5 and IL-13, which augment allergic inflammation. However, little information is currently available about the induction of these responses by the respiratory viruses that are strongly associated with exacerbations of asthma, such as rhinoviruses. Further human studies, as well as improved animal experimental models, are needed to investigate appropriately the pathogenetic mechanisms in virus-induced exacerbations of asthma, including the role of ILCs.
哮喘急性加重最常见的诱因是病毒感染，病毒感染会加剧过敏性炎症。病毒感染的气道上皮细胞（AECs）释放的细胞因子可能在驱动这种反应中起重要作用。本综述重点关注越来越多的证据，这些证据支持上皮细胞因子（包括白细胞介素-33（IL-33）、白细胞介素-25（IL-25）和胸腺基质淋巴细胞生成素（TSLP））及其靶标2型固有淋巴细胞（ILC2s）在病毒诱导的哮喘急性加重发病机制中的作用。这些细胞因子的产生和释放导致ILC2s的募集和激活，ILC2s分泌包括白细胞介素-5（IL-5）和白细胞介素-13（IL-13）在内的介质，从而加剧过敏性炎症。然而，目前关于与哮喘急性加重密切相关的呼吸道病毒（如鼻病毒）诱导这些反应的信息很少。需要进一步的人体研究以及改进的动物实验模型，以适当研究病毒诱导的哮喘急性加重的发病机制，包括ILCs的作用。
