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Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
A novel outbred mouse model of 2009 pandemic influenza and bacterial co-infection severity
Kevin J McHugh1, Sivanarayana Mandalapu, Jay K Kolls
1Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania, United States of America.
Abstract:
Influenza viruses pose a significant health risk and annually impose a great cost to patients and the health care system. The molecular determinants of influenza severity, often exacerbated by secondary bacterial infection, are largely unclear. We generated a novel outbred mouse model of influenza virus, Staphylococcus aureus, and co-infection utilizing influenza A/CA/07/2009 virus and S. aureus (USA300). Outbred mice displayed a wide range of pathologic phenotypes following influenza virus or co-infection ranging broadly in severity. Influenza viral burden positively correlated with weight loss although lung histopathology did not. Inflammatory cytokines including IL-6, TNF-α, G-CSF, and CXCL10 positively correlated with both weight loss and viral burden. In S. aureus infection, IL-1β, G-CSF, TNF-α, and IL-6 positively correlated with weight loss and bacterial burden. In co-infection, IL-1β production correlated with decreased weight loss suggesting a protective role. The data demonstrate an approach to identify biomarkers of severe disease and to understand pathogenic mechanisms in pneumonia.
Insights
This study introduces a new mouse model for influenza and Staphylococcus aureus co-infection. The model helps identify biomarkers for severe pneumonia and understand infection mechanisms.
Area of Science:
- Infectious Diseases
- Immunology
- Microbiology
Background:
- Influenza viruses cause significant health burdens annually.
- Understanding factors influencing influenza severity, especially with secondary bacterial infections, remains a challenge.
Purpose of the Study:
- To develop a novel outbred mouse model for influenza and Staphylococcus aureus co-infection.
- To identify molecular determinants and biomarkers associated with disease severity in respiratory infections.
Main Methods:
- Utilized influenza A/CA/07/2009 virus and Staphylococcus aureus (USA300) in an outbred mouse model.
- Assessed pathological phenotypes, viral and bacterial burden, and inflammatory cytokine profiles (IL-6, TNF-α, G-CSF, CXCL10, IL-1β).
Main Results:
- Outbred mice exhibited varied pathological responses to influenza or co-infection.
- Influenza viral burden correlated with weight loss and specific cytokine levels.
- Interleukin-1β (IL-1β) production in co-infection showed a protective effect, correlating with decreased weight loss.
Conclusions:
- The developed mouse model effectively simulates influenza and bacterial co-infection, revealing diverse disease severities.
- Identified correlations between cytokine profiles, pathogen burden, and clinical outcomes.
- Suggests a potential protective role for IL-1β in co-infection, offering insights into pathogenic mechanisms.
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