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Open Access Letter to the Editor

Airway protease/antiprotease imbalance in atopic asthmatics contributes to increased Influenza A virus cleavage and replication

Matthew J Kesic15, Michelle Hernandez123 and Ilona Jaspers1234*

Author Affiliations

1 Center for Environmental Medicine, Asthma, and Lung Biology, School of Medicine, University of North Carolina at Chapel Hill, 104 Mason Farm Rd; CB# 7310, Chapel Hill, NC, 27599-7310, USA

2 The Curriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

3 The Department of Pediatrics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

4 The Department of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

5 The Department of Biology, Methodist University, Fayetteville, NC, USA

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Respiratory Research 2012, 13:82  doi:10.1186/1465-9921-13-82

Published: 19 September 2012

Abstract

Asthmatics are more susceptible to influenza infections, yet mechanisms mediating this enhanced susceptibility are unknown. Influenza virus hemagglutinin (HA) protein binds to sialic acid residues on the host cells. HA requires cleavage to allow fusion of the viral HA with host cell membrane, which is mediated by host trypsin-like serine protease. We show data here demonstrating that the protease:antiprotease ratio is increased in the nasal mucosa of asthmatics and that these changes were associated with increased proteolytic activation of influenza. These data suggest that disruption of the protease balance in asthmatics enhances activation and infection of influenza virus.

Keywords:
Asthma; Influenza A; Protease; Antiprotease; SLPI; TMPRSS2; Hemagglutinin; Susceptibility