tetano
Editor, Senior Moderator
Mucosal Immunol. 2017 Apr 12. doi: 10.1038/mi.2017.32. [Epub ahead of print]
[h=1]Novel protective mechanism for interleukin-33 at the mucosal barrier during influenza-associated bacterial superinfection.[/h] Robinson KM[SUP]1[/SUP], Ramanan K[SUP]2[/SUP], Clay ME[SUP]2,[/SUP][SUP]3[/SUP], McHugh KJ[SUP]2[/SUP], Rich HE[SUP]2[/SUP], Alcorn JF[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A is a highly contagious respiratory virus that causes seasonal epidemics and occasional worldwide pandemics. The primary cause of influenza-related mortality is bacterial superinfection. There are numerous mechanisms by which preceding influenza infection attenuates host defense, allowing for increased susceptibility to bacterial pneumonia. Herein, we demonstrate that influenza inhibits Staphylococcus aureus-induced production of interleukin-33 (IL-33). Restoration of IL-33 during influenza A and methicillin-resistant S. aureus superinfection enhanced bacterial clearance and improved mortality. Innate lymphoid Type 2 cells and alternatively activated macrophages are not required for IL-33-mediated protection during superinfection. We show that IL-33 treatment resulted in neutrophil recruitment to the lung, associated with improved bacterial clearance. These findings identify a novel role for IL-33 in antibacterial host defense at the mucosal barrier.Mucosal Immunology advance online publication, 12 April 2017; doi:10.1038/mi.2017.32.
PMID: 28401938 DOI: 10.1038/mi.2017.32
[h=1]Novel protective mechanism for interleukin-33 at the mucosal barrier during influenza-associated bacterial superinfection.[/h] Robinson KM[SUP]1[/SUP], Ramanan K[SUP]2[/SUP], Clay ME[SUP]2,[/SUP][SUP]3[/SUP], McHugh KJ[SUP]2[/SUP], Rich HE[SUP]2[/SUP], Alcorn JF[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A is a highly contagious respiratory virus that causes seasonal epidemics and occasional worldwide pandemics. The primary cause of influenza-related mortality is bacterial superinfection. There are numerous mechanisms by which preceding influenza infection attenuates host defense, allowing for increased susceptibility to bacterial pneumonia. Herein, we demonstrate that influenza inhibits Staphylococcus aureus-induced production of interleukin-33 (IL-33). Restoration of IL-33 during influenza A and methicillin-resistant S. aureus superinfection enhanced bacterial clearance and improved mortality. Innate lymphoid Type 2 cells and alternatively activated macrophages are not required for IL-33-mediated protection during superinfection. We show that IL-33 treatment resulted in neutrophil recruitment to the lung, associated with improved bacterial clearance. These findings identify a novel role for IL-33 in antibacterial host defense at the mucosal barrier.Mucosal Immunology advance online publication, 12 April 2017; doi:10.1038/mi.2017.32.
PMID: 28401938 DOI: 10.1038/mi.2017.32