Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 44, Issue 11, Pages 3263-3272Publisher
WILEY
DOI: 10.1002/eji.201444582
Keywords
IFN- IL-13 Influenza Methicillin-resistant Staphylococcus aureus (MRSA) Secondary-bacterial infections
Categories
Funding
- National Institute of Allergy and Infectious Diseases at National Institutes of Health [1R56AI089458, R01AI04905]
- IDeA Networks for Biomedical Research Excellence at National Institutes of Health [P20GM103474]
- Centers for Biomedical Research Excellence at National Institutes of Health [P20GM103500]
- National Institutes of Health IDeA Program [GM110732]
- Montana State University Agricultural Experiment Station
- M.J. Murdock Charitable Trust
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Superinfection in mice at day 7 postinfluenza infection exacerbates bacterial pneumonia at least in part via downstream effects of increased IFN-signaling. Here we show that up to 3 days postinfluenza infection, mice have reduced susceptibility to superinfection with methicillin-resistant Staphylococcus aureus (MRSA), but that superinfection during that time exacerbated influenza disease. This was due to IL-13 signaling that was advantageous for resolving MRSA infection via inhibition of IFN-, but was detrimental to the clearance of influenza virus. However, if superinfection did not occur until the near resolution of influenza infection (day 7), IL-13 signaling was inhibited, at least in part by upregulation of IL-13 decoy receptor (IL-13R2), which in turn caused increases in IFN- signaling and exacerbation of bacterial infection. Understanding these cytokine sequelae is critical to development of immunotherapies for influenza-MRSA coinfection since perturbations of these sequelae at the wrong time could increase susceptibility to MRSA and/or influenza.
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