The cell surface mucin MUC1 limits the severity of influenza A virus infection
In: Mucosal Immunology, Jg. 10 (2017-11-01), S. 1581-1593
Online
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Zugriff:
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 cells, we found that IAV associates with the cs-mucin MUC1 but not MUC13 or MUC16. Overexpression of MUC1 by epithelial cells or the addition of sialylated synthetic MUC1 constructs, reduced IAV infection in vitro. In addition, Muc1-/- mice infected with IAV exhibited enhanced morbidity and mortality, as well as greater inflammatory mediator responses compared to wild type mice. This study implicates the cs-mucin MUC1 as a critical and dynamic component of the innate host response that limits the severity of influenza and provides the foundation for exploration of MUC1 in resolving inflammatory disease.
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The cell surface mucin MUC1 limits the severity of influenza A virus infection
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Autor/in / Beteiligte Person: | Brown, Lorena E. ; McGuckin, Michael A. ; McAuley, Julie L. ; Corcilius, Leo ; Tan, Hyon-Xhi ; Payne, Richard J. |
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Zeitschrift: | Mucosal Immunology, Jg. 10 (2017-11-01), S. 1581-1593 |
Veröffentlichung: | Elsevier BV, 2017 |
Medientyp: | unknown |
ISSN: | 1933-0219 (print) |
DOI: | 10.1038/mi.2017.16 |
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