tetano
Editor, Senior Moderator
Virology. 2016 Sep 12;499:23-29. doi: 10.1016/j.virol.2016.08.025. [Epub ahead of print]
[h=1]Influenza virus infection causes neutrophil dysfunction through reduced G-CSF production and an increased risk of secondary bacteria infection in the lung.[/h] Ishikawa H[SUP]1[/SUP], Fukui T[SUP]2[/SUP], Ino S[SUP]1[/SUP], Sasaki H[SUP]3[/SUP], Awano N[SUP]2[/SUP], Kohda C[SUP]1[/SUP], Tanaka K[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The immunological mechanisms of secondary bacterial infection followed by influenza virus infection were examined. When mice were intranasally infected with influenza virus A and then infected with P. aeruginosa at 4 days after viral infection, bacterial clearance in the lung significantly decreased compared to that of non-viral infected mice. Neutrophils from viral infected mice showed impaired digestion and/or killing of phagocytized bacteria due to reduced myeloperoxidase (MPO) activity. G-CSF production in the lungs of viral infected mice was lower than that of non-viral infected mice after secondary bacterial infection. When viral infected mice were injected with G-CSF before secondary bacterial infection, the MPO activity of viral infected mice restored to the same level as that of non-infected mice. Bacteria clearance in viral infected mice was also recovered by G-CSF administration. Thus, neutrophil dysfunction caused by influenza virus is attributed to insufficient G-CSF production, which induces a secondary bacterial infection.
Copyright ? 2016 Elsevier Inc. All rights reserved.
[h=4]KEYWORDS:[/h] G-CSF; Influenza virus; Neutrophil; P. aeruginosa
PMID: 27632562 DOI: 10.1016/j.virol.2016.08.025
[PubMed - as supplied by publisher]
[h=1]Influenza virus infection causes neutrophil dysfunction through reduced G-CSF production and an increased risk of secondary bacteria infection in the lung.[/h] Ishikawa H[SUP]1[/SUP], Fukui T[SUP]2[/SUP], Ino S[SUP]1[/SUP], Sasaki H[SUP]3[/SUP], Awano N[SUP]2[/SUP], Kohda C[SUP]1[/SUP], Tanaka K[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The immunological mechanisms of secondary bacterial infection followed by influenza virus infection were examined. When mice were intranasally infected with influenza virus A and then infected with P. aeruginosa at 4 days after viral infection, bacterial clearance in the lung significantly decreased compared to that of non-viral infected mice. Neutrophils from viral infected mice showed impaired digestion and/or killing of phagocytized bacteria due to reduced myeloperoxidase (MPO) activity. G-CSF production in the lungs of viral infected mice was lower than that of non-viral infected mice after secondary bacterial infection. When viral infected mice were injected with G-CSF before secondary bacterial infection, the MPO activity of viral infected mice restored to the same level as that of non-infected mice. Bacteria clearance in viral infected mice was also recovered by G-CSF administration. Thus, neutrophil dysfunction caused by influenza virus is attributed to insufficient G-CSF production, which induces a secondary bacterial infection.
Copyright ? 2016 Elsevier Inc. All rights reserved.
[h=4]KEYWORDS:[/h] G-CSF; Influenza virus; Neutrophil; P. aeruginosa
PMID: 27632562 DOI: 10.1016/j.virol.2016.08.025
[PubMed - as supplied by publisher]