title: Respiratory viral infection, epithelial cytokines, and innate lymphoid cells in asthma exacerbations.
abstract: 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.
authors.affiliation: Department of Pathology, University of New South Wales, Sydney, Australia; r.kumar@unsw.edu.au.
authors.forename: Rakesh K
authors.initials: RK
authors.lastname: Kumar
authors.affiliation: Centre for Asthma and Respiratory Disease, University of Newcastle and Hunter Medical Research Institute, Callaghan, Australia; and.
authors.forename: Paul S
authors.initials: PS
authors.lastname: Foster
authors.affiliation: Inflammation Immunobiology Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
authors.forename: Helene F
authors.initials: HF
authors.lastname: Rosenberg
mesh_terms: D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D003713:Dendritic Cells / Q000276:immunology; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000378:metabolism* / Q000821:virology; D005786:Gene Expression Regulation; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation; D007378:Interleukins / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D008214:Lymphocytes / Q000378:metabolism / Q000502:physiology*; D051379:Mice; D010850:Picornaviridae Infections / Q000150:complications / Q000276:immunology; D012107:Research Design; D018357:Respiratory Syncytial Virus Infections / Q000150:complications / Q000276:immunology; D012137:Respiratory System / Q000473:pathology; D012141:Respiratory Tract Infections / Q000150:complications* / Q000276:immunology; D012229:Rhinovirus; D014777:Virus Diseases / Q000150:complications* / Q000276:immunology; D000094632:Thymic Stromal Lymphopoietin
chemical_list: D016207:Cytokines; D007378:Interleukins; D000094632:Thymic Stromal Lymphopoietin
keywords: Th2; allergy; animal models; interleukin-33