Regulation of IFN-γ by IL-13 Dictates the Susceptibility to Secondary Post-Influenza MRSA Pneumonia
| Autor: | Rynda-Apple, Agnieszka, Harmsen, Ann, Erickson, Anfin S., Larson, Kyle, Morton, Rachelle V., Richert, Laura E., Harmsen, Allen G. |
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| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
Methicillin-Resistant Staphylococcus aureus
Mice Knockout Mice Inbred BALB C Interleukin-13 Coinfection virus diseases Staphylococcal Infections Viral Load Article Bacterial Load Recombinant Proteins Mice Inbred C57BL Interferon-gamma Mice Orthomyxoviridae Infections Superinfection Interleukin-13 Receptor alpha2 Subunit Pneumonia Bacterial Animals Disease Susceptibility Lung |
| Popis: | Super infection in mice at day 7 post-influenza infection exacerbates bacterial pneumonia at least in part via downstream effects of increased IFN-γ signaling. Here we show that up to 3 days post-influenza infection mice have reduced susceptibility to super infection with methicillin-resistant Staphylococcus aureus (MRSA), but that super infection during that time exacerbated influenza disease. This was due to IL-13 signaling that was advantageous for resolving MRSA infection via inhibition of IFN-γ, but was detrimental to clearance of influenza virus. However, if super infection did not occur until the near resolution of influenza infection (day 7), IL-13 signaling was inhibited, at least in part by up regulation of IL-13 decoy receptor (IL-13Rα2), which in turn caused increases in IFN-γ 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. |
| Databáze: | OpenAIRE |
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