IL-17E (IL-25) and IL-17RB promote respiratory syncytial virus-induced pulmonary disease. Issue 5 (9th January 2014)

• Record Type: Journal Article
• Authors: Petersen, Bryan C; Dolgachev, Vladislav; Rasky, Andrew; Lukacs, Nicholas W
• Is Part Of: Journal of leukocyte biology. Volume 95:Issue 5(2014)
• Page Start: 809
• Page End: 815
• Publication Date: 2014-01-09
• Subjects: mucus -- Th2 -- cytokines; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1189/jlb.0913482
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract : RSV infection induces IL-25 that contributes to the pathogenesis of pulmonary disease during primary infection and asthma-like exacerbations. ABSTRACT: One of the most severe pathologic responses of RSV infection is associated with overproduction of cytokines and inflammation, leading to mucus hypersecretion. This study investigated the role of IL-25 in the development of RSV-associated immunopathology. IL-25 and its receptor IL-17RB were increased following RSV infection, and IL-25 blockade using neutralizing antibodies reduced RSV-associated pathology, AHR, and type 2 cytokine production. Likewise, IL-17RB −/− mice demonstrated a modified inflammatory response during RSV infection characterized by decreased Th2 and increased Th17 cytokine production. Additionally, the IL-17RB −/− mice demonstrated significantly reduced inflammation and cytokine production in a model of RSV-driven asthma exacerbation. These results indicate that IL-25 regulates the inflammatory response to RSV infection and that its inhibition may enable a reduction in the severity of RSV-associated pulmonary inflammation, including during viral-induced asthma exacerbation.