Respiratory viral infection, epithelial cytokines, and innate lymphoid cells in asthma exacerbations

• Published in: Journal of leukocyte biology Vol. 96; no. 3; pp. 391 - 396
• Main Authors: Kumar, Rakesh K., Foster, Paul S., Rosenberg, Helene F.
• Format: Journal Article
• Language: English
• Published: United States Society for Leukocyte Biology 01-09-2014
• Subjects: allergy; animal models; Animals; Asthma - etiology; Asthma - immunology; Cytokines - biosynthesis; Cytokines - genetics; Cytokines - physiology; Cytokines - secretion; Dendritic Cells - immunology; Disease Models, Animal; Epithelial Cells - secretion; Epithelial Cells - virology; Gene Expression Regulation; Humans; Immunity, Innate; Inflammation; Interleukins - biosynthesis; Interleukins - genetics; Interleukins - secretion; interleukin‐33; Lymphocytes - physiology; Lymphocytes - secretion; Mice; Picornaviridae Infections - complications; Picornaviridae Infections - immunology; Research Design; Respiratory Syncytial Virus Infections - complications; Respiratory Syncytial Virus Infections - immunology; Respiratory System - pathology; Respiratory Tract Infections - complications; Respiratory Tract Infections - immunology; Reviews; Rhinovirus; Th2; Virus Diseases - complications; Virus Diseases - immunology; allergy; animal models; interleukin-33; Th2
• ISSN: 0741-5400; 1938-3673
• DOI: 10.1189/jlb.3RI0314-129R

Review of how viral infection of airway epithelial cells leading to release of Th2‐promoting cytokines may drive asthma exacerbations via activation of innate lymphoid cells.
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.