The cell surface mucin MUC1 limits the severity of influenza A virus infection

JL McAuley; L Corcilius; HX Tan; RJ Payne; MA McGuckin; LE Brown

Journal article

The cell surface mucin MUC1 limits the severity of influenza A virus infection

JL McAuley, L Corcilius, HX Tan, RJ Payne, MA McGuckin, LE Brown

Mucosal Immunology | NATURE PUBLISHING GROUP | Published : 2017

DOI: 10.1038/mi.2017.16

Abstract

Cell surface mucin (cs-mucin) glycoproteins are constitutively expressed at the surface of respiratory epithelia where pathogens such as influenza A virus (IAV) gain entry into cells. Different members of the cs-mucin family each express a large and heavily glycosylated extracellular domain that towers above other receptors on the epithelial cell surface, a transmembrane domain that enables shedding of the extracellular domain, and a cytoplasmic tail capable of triggering signaling cascades. We hypothesized that IAV can interact with the terminal sialic acids presented on the extracellular domain of cs-mucins, resulting in modulation of infection efficiency. Utilizing human lung epithelial c..

View full abstract

University of Melbourne Researchers

Related Projects (2)

LIMITING THE IMPACT OF INFLUENZA

The development of better ways to prevent and treat influenza infection will be a major step forward in lessening the impact of the virus in..

PB1-F2 IS CRITICAL TO INFLUENZA A VIRUS PATHOGENICITY THROUGH ACTIVATION OF THE INFLAMMASOME

Fatal Influenza A virus infections are excessive inflammation. We identified the IAV protein PB1-F2 as critical in driving excessive inflamm..

Grants

Awarded by Australian Research Council

Funding Acknowledgements

J.M. is funded by the National Health and Medical Research Council of Australia (NHMRC) Project Grant 1079924; H.X.T. receives the Australian Postgraduate Award for PhD salary support. L.B. receives funding from NHMRC Program Grant 1071916. R.P. acknowledges the Australian Research Council for Discovery Project funding (DP120100194). L.C. also acknowledges John A. Lamberton Scholarship for PhD funding. M.M. is supported by a Senior Research Fellowships from the NHMRC. We acknowledge St Jude Children's Research Hospital, (TN, USA) as the original source of the PR8 plasmids used to reverse engineer and generate the IAV used in this study. We also acknowledge the Biological Optical Microscopy Platform at the University of Melbourne for use and maintenance of the confocal microscopy suite.