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Novel protective mechanism for interleukin-33 at the mucosal barrier during
influenza-associated bacterial superinfection
#MMPMID28401938
Robinson KM
; Ramanan K
; Clay ME
; McHugh KJ
; Rich HE
; Alcorn JF
Mucosal Immunol
2018[Jan]; 11
(1
): 199-208
PMID28401938
show ga
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.
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