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Updated: May 30, 2026
Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
Limited effects of Muc1 deficiency on mouse adenovirus type 1 respiratory infection
Y Nguyen1, Megan C Procario, Shanna L Ashley
1Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI, United States. Y.Nguyen@UTSouthwestern.edu
Abstract:
Muc1 (MUC1 in humans) is a membrane-tethered mucin that exerts anti-inflammatory effects in the lung during bacterial infection. Muc1 and other mucins are also likely to form a protective barrier in the lung. We used mouse adenovirus type 1 (MAV-1, also known as MAdV-1) to determine the role of Muc1 in the pathogenesis of an adenovirus in its natural host. Following intranasal inoculation of wild type mice, we detected increased TNF-α, a cytokine linked to Muc1 production, but no consistent changes in the production of lung Muc1, Muc5ac or overall lung mucus production. Viral loads were modestly higher in the lungs of Muc1(-/-) mice compared to Muc1(+/+) mice at several early time points but decreased to similar levels by 14 days post infection in both groups. However, cellular inflammation and the expression of CXCL1, CCL5, and CCL2 did not significantly differ between Muc1(-/-) and Muc1(+/+) mice. Our data therefore suggest that Muc1 may contribute to a physical barrier that protects against MAV-1 respiratory infection. However, our data do not reveal an anti-inflammatory effect of Muc1 that contributes to MAV-1 pathogenesis.
Insights
Muc1 (MUC1 in humans) may act as a physical barrier protecting the lungs against mouse adenovirus type 1 (MAV-1). This study found no evidence of an anti-inflammatory role for Muc1 during MAV-1 infection.
Area of Science:
- Immunology
- Respiratory Medicine
- Virology
Background:
- Mucin 1 (Muc1) is a membrane-tethered mucin known for anti-inflammatory effects in bacterial lung infections.
- Mucins, including Muc1, are hypothesized to form a protective barrier in the respiratory tract.
- The specific role of Muc1 in viral pathogenesis, particularly adenovirus, remains underexplored.
Purpose of the Study:
- To investigate the role of Muc1 in the pathogenesis of mouse adenovirus type 1 (MAV-1) infection in its natural host.
- To determine if Muc1 influences viral load, inflammatory responses, or cytokine production during MAV-1 infection.
- To elucidate the contribution of Muc1 to host defense mechanisms against respiratory viral infections.
Main Methods:
- Intranasal inoculation of wild-type and Muc1-deficient (Muc1(-/-)) mice with MAV-1.
- Quantification of viral loads in lung tissue at various time points post-infection.
- Measurement of inflammatory cytokines (e.g., TNF-α) and chemokines (e.g., CXCL1, CCL5, CCL2) in lung tissue.
- Assessment of cellular inflammation and overall mucus production.
Main Results:
- Elevated TNF-α levels were observed post-infection, correlating with Muc1 production, but Muc1, Muc5ac, and overall mucus levels did not consistently change.
- Viral loads were transiently higher in Muc1(-/-) mice compared to wild-type mice early in infection, but normalized by 14 days.
- No significant differences in cellular inflammation or expression of CXCL1, CCL5, and CCL2 were detected between Muc1(-/-) and wild-type mice.
Conclusions:
- Muc1 appears to contribute to a physical barrier that offers protection against MAV-1 respiratory infection.
- The study did not find evidence supporting an anti-inflammatory role for Muc1 in the context of MAV-1 pathogenesis.
- Further research is needed to fully understand Muc1's complex role in viral respiratory infections.
