| First Author | McAuley JL | Year | 2017 |
| Journal | Mucosal Immunol | Volume | 10 |
| Issue | 6 | Pages | 1581-1593 |
| PubMed ID | 28327617 | Mgi Jnum | J:345124 |
| Mgi Id | MGI:6838156 | Doi | 10.1038/mi.2017.16 |
| Citation | McAuley JL, et al. (2017) The cell surface mucin MUC1 limits the severity of influenza A virus infection. Mucosal Immunol 10(6):1581-1593 |
| abstractText | 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. |
