tetano
Editor, Senior Moderator
Antiviral Res. 2015 Apr 28. pii: S0166-3542(15)00103-5. doi: 10.1016/j.antiviral.2015.04.011. [Epub ahead of print]
[h=1]Mitochondrial reactive oxygen species modulate innate immune response to influenza A virus in human nasal epithelium.[/h] Kim S[SUP]1[/SUP], Kim MJ[SUP]1[/SUP], Park DY[SUP]2[/SUP], Chung HJ[SUP]2[/SUP], Kim CH[SUP]3[/SUP], Yoon JH[SUP]4[/SUP], Kim HJ[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The innate immune system of the nasal epithelium serves as a first line of defense against invading respiratory viruses including influenza A virus (IAV). Recently, it was verified that interferon (IFN)-related immune responses play a critical role in local antiviral innate immunity. Reactive oxygen species (ROS) generation by exogenous pathogens has also been demonstrated in respiratory epithelial cells and modulation of ROS has been reported to be important for respiratory virus-induced innate immune mechanisms. Passage-2 normal human nasal epithelial (NHNE) cells were inoculated with IAV (WS/33, H1N1) to assess the sources of IAV-induced ROS and the relationship between ROS and IFN-related innate immune responses. Both STAT1 and STAT2 phosphorylation and the mRNA levels of IFN-stimulated genes, including Mx1, 2,5-OAS1, IFIT1, and CXCL10, were induced after IAV infection up to three days post infection. Similarly, we observed that mitochondrial ROS generation increased maximally at 2days after IAV infection. After suppression of mitochondrial ROS generation, IAV-induced phosphorylation of STAT and mRNA levels of IFN-stimulated genes were attenuated and actually, viral titers of IAV were significantly higher in cases with scavenging ROS. Our findings suggest that mitochondrial ROS might be responsible for controlling IAV infection and may be potential sources of ROS generation, which is required to initiate an innate immune response in NHNE cells.
Copyright ? 2015. Published by Elsevier B.V.
[h=4]KEYWORDS:[/h] Influenza A virus; Interferon-stimulated genes; Mitochondria; Reactive oxygen species
PMID: 25930096 [PubMed - as supplied by publisher]
[h=1]Mitochondrial reactive oxygen species modulate innate immune response to influenza A virus in human nasal epithelium.[/h] Kim S[SUP]1[/SUP], Kim MJ[SUP]1[/SUP], Park DY[SUP]2[/SUP], Chung HJ[SUP]2[/SUP], Kim CH[SUP]3[/SUP], Yoon JH[SUP]4[/SUP], Kim HJ[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The innate immune system of the nasal epithelium serves as a first line of defense against invading respiratory viruses including influenza A virus (IAV). Recently, it was verified that interferon (IFN)-related immune responses play a critical role in local antiviral innate immunity. Reactive oxygen species (ROS) generation by exogenous pathogens has also been demonstrated in respiratory epithelial cells and modulation of ROS has been reported to be important for respiratory virus-induced innate immune mechanisms. Passage-2 normal human nasal epithelial (NHNE) cells were inoculated with IAV (WS/33, H1N1) to assess the sources of IAV-induced ROS and the relationship between ROS and IFN-related innate immune responses. Both STAT1 and STAT2 phosphorylation and the mRNA levels of IFN-stimulated genes, including Mx1, 2,5-OAS1, IFIT1, and CXCL10, were induced after IAV infection up to three days post infection. Similarly, we observed that mitochondrial ROS generation increased maximally at 2days after IAV infection. After suppression of mitochondrial ROS generation, IAV-induced phosphorylation of STAT and mRNA levels of IFN-stimulated genes were attenuated and actually, viral titers of IAV were significantly higher in cases with scavenging ROS. Our findings suggest that mitochondrial ROS might be responsible for controlling IAV infection and may be potential sources of ROS generation, which is required to initiate an innate immune response in NHNE cells.
Copyright ? 2015. Published by Elsevier B.V.
[h=4]KEYWORDS:[/h] Influenza A virus; Interferon-stimulated genes; Mitochondria; Reactive oxygen species
PMID: 25930096 [PubMed - as supplied by publisher]