|作者：||Khoo Siew-Kim, Read James, Franks Kimberley, Zhang Guicheng, Bizzintino Joelene, Coleman Laura, McCrae Christopher, Öberg Lisa, Troy Niamh M, Prastanti Franciska, Everard Janet, Oo Stephen, Borland Meredith L, Maciewicz Rose A, Le Souëf Peter N, Laing Ingrid A, Bosco Anthony|
1Division of Cardiovascular and Respiratory Sciences, The University of Western Australia, Perth, Western Australia 6009, Australia.
2Telethon Kids Institute, The University of Western Australia, Perth, Western Australia 6008, Australia.
3School of Public Health, Curtin University, Perth, Western Australia 6102, Australia.
4Centre for Genetic Origins of Health and Disease, The University of Western Australia, Perth, Western Australia 6009, Australia and Curtin University, Perth, Western Australia 6102, Australia.
5Division of Cardiovascular an
|刊名：||Journal of immunology (Baltimore, Md. : 1950), 2019|
|原始语种摘要：||Asthma exacerbations are triggered by rhinovirus infections. We employed a systems biology approach to delineate upper-airway gene network patterns underlying asthma exacerbation phenotypes in children. Cluster analysis unveiled distinct IRF7hi versus IRF7lo molecular phenotypes, the former exhibiting robust upregulation of Th1/type I IFN responses and the latter an alternative signature marked by upregulation of cytokine and growth factor signaling and downregulation of IFN-γ. The two phenotypes also produced distinct clinical phenotypes. For IRF7lo children, symptom duration prior to hospital presentation was more than twice as long from initial symptoms ( p = 0.011) and nearly three times as long for cough ( p < 0.001), the odds ratio of admission to hospital was increased more than... 4-fold ( p = 0.018), and time to recurrence was shorter ( p = 0.015). In summary, our findings demonstrate that asthma exacerbations in children can be divided into IRF7hi versus IRF7lo phenotypes with associated differences in clinical phenotypes.|