TGF-β production associated with allergic asthma prevents influenza virus induced immunopathology (VIR5P.1160)

Abstract

Abstract Asthma is believed to be a risk factor for influenza infection, however little remains known about how the asthmatic phenotype influences anti-viral immune responses. We therefore investigated the impact of asthma on susceptibility to influenza infection by using a mouse model of allergic airway inflammation. Unexpectedly, asthmatic mice were highly resistant to primary infection with the H1N1 2009 pandemic strain. Notably, the increased resistance was not attributed to enhanced viral clearance but instead was due to reduced lung inflammation. Asthmatic mice exhibited a significantly reduced cytokine storm as well as reduced total protein levels and cytotoxicity in the airways, indicators of decreased tissue injury. Further, we show that asthmatic mice have significantly increased levels of TGF-β1 and that the heightened resistance of asthmatic mice is abrogated in the absence of TGF-β receptor II. Thus, we conclude that the transient increase in TGF-β expression following an acute asthma episode is responsible for temporarily protection via suppression of influenza-induced immunopathology.