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Updated: Mar 5, 2026
Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein
Published on: April 21, 2015
The cell surface mucin MUC1 limits the severity of influenza A virus infection
J L McAuley1, L Corcilius2, H-X Tan1
1Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia.
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 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.
Insights
Cell surface mucin MUC1 limits influenza A virus infection by binding sialic acids. MUC1-deficient mice show increased illness and inflammation, highlighting MUC1's role in host defense.
Area of Science:
- Respiratory Virology
- Glycobiology
- Innate Immunity
Background:
- Cell surface mucins (cs-mucins) like MUC1 are expressed on respiratory epithelia, serving as entry points for pathogens such as influenza A virus (IAV).
- These mucins possess heavily glycosylated extracellular domains presenting terminal sialic acids, which could interact with viral particles.
Purpose of the Study:
- To investigate the hypothesis that IAV interacts with cs-mucins, modulating influenza infection efficiency.
- To determine the specific role of MUC1 in the host response to IAV infection.
Main Methods:
- Utilized human lung epithelial cells to assess IAV association with MUC1, MUC13, and MUC16.
- Employed overexpression of MUC1 and addition of sialylated MUC1 constructs to evaluate effects on IAV infection in vitro.
- Infected Muc1 knockout (Muc1-/-) and wild-type mice with IAV to compare morbidity, mortality, and inflammatory responses.
Main Results:
- IAV was found to associate with MUC1, but not MUC13 or MUC16, on human lung epithelial cells.
- Overexpression of MUC1 or addition of MUC1 constructs reduced IAV infection in vitro.
- Muc1-/- mice exhibited increased morbidity, mortality, and inflammatory mediator release upon IAV infection compared to wild-type controls.
Conclusions:
- The cell surface mucin MUC1 is a key component of the innate immune response against influenza A virus.
- MUC1 limits influenza severity and suggests its potential therapeutic role in managing inflammatory diseases.
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