tetano
Editor, Senior Moderator
ur J Immunol. 2014 Aug 4. doi: 10.1002/eji.201444582. [Epub ahead of print]
Regulation of IFN-γ by IL-13 dictates susceptibility to secondary post-Influenza MRSA pneumonia.
Rynda-Apple A1, Harmsen A, Erickson AS, Larson K, Morton RV, Richert LE, Harmsen AG.
Author information
Abstract
Superinfection 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 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-γ, 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-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. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
IFN-γ; IL-13; Influenza; methicillin-resistant Staphylococcus aureus (MRSA); secondary-bacterial infections
PMID:
25091976
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25091976
Regulation of IFN-γ by IL-13 dictates susceptibility to secondary post-Influenza MRSA pneumonia.
Rynda-Apple A1, Harmsen A, Erickson AS, Larson K, Morton RV, Richert LE, Harmsen AG.
Author information
Abstract
Superinfection 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 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-γ, 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-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. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
IFN-γ; IL-13; Influenza; methicillin-resistant Staphylococcus aureus (MRSA); secondary-bacterial infections
PMID:
25091976
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25091976