tetano
Editor, Senior Moderator
Am J Respir Cell Mol Biol. 2013 Jun 20. [Epub ahead of print]
ROS Induce Antiviral Innate Immune Response through Interferon-λ Regulation in Human Nasal Epithelial Cells.
Kim HJ, Kim CH, Ryu JH, Kim MJ, Park CY, Lee JM, Holtzman MJ, Yoon JH.
Source
Chung-Ang University College of Medicine, Department of Otolaryngology and Head & Neck Surgery, Seoul, Korea, Republic of ; hyunjk@cau.ac.kr.
Abstract
The goals of this study were to explore the role of interferon (IFN)-related innate immune response (IFN-?, IFN-λ) and reactive oxygen species (ROS) after influenza A virus (IAV) infection for antiviral innate immune activity in normal human nasal epithelial (NHNE) cells that are highly exposed to IAV. Passage-2 NHNE cells were inoculated with the IAV WSN/33 for 1, 2, and 3 days to assess the capacity of IFN and the relationship between ROS-generation and IFN-λ secretion, for controlling IAV infection. Viral titer and IAV mRNA level increased after infection. In concert with viral titer, we found that generation of IFNs, such as IFN-?, IFN-λ1 and IFN-λ2/3 was induced after IAV infection until three days post of infection (PI). Induction of IFN-λ-gene expression and protein secretion might be predominant after IAV infection. Similarly, we observed that intracellular ROS generation increased 60 minutes after IAV infection. Viral titer and mRNA level of IAV were significantly higher in cases with scavenging ROS, in cases with an induced IFN-λ mRNA level or where secreted protein concentration of IFN-λ was attenuated after suppression of ROS generation. Both mitochondrial and Duox2-generated ROS were correlated with IAV mRNA and viral titer. Inhibition of mitochondrial ROS generation and knock-down of Duox2 gene expression highly increased IAV viral titer and decreased IFN-λ secretion. Our findings suggest that production of ROS might be responsible for IFN-λ secretion to control IAV infection. Both mitochondria and Duox2 are possible sources of ROS generation, which is required to initiate an innate immune response in NHNE cells.
PMID:
23786562
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23786562
ROS Induce Antiviral Innate Immune Response through Interferon-λ Regulation in Human Nasal Epithelial Cells.
Kim HJ, Kim CH, Ryu JH, Kim MJ, Park CY, Lee JM, Holtzman MJ, Yoon JH.
Source
Chung-Ang University College of Medicine, Department of Otolaryngology and Head & Neck Surgery, Seoul, Korea, Republic of ; hyunjk@cau.ac.kr.
Abstract
The goals of this study were to explore the role of interferon (IFN)-related innate immune response (IFN-?, IFN-λ) and reactive oxygen species (ROS) after influenza A virus (IAV) infection for antiviral innate immune activity in normal human nasal epithelial (NHNE) cells that are highly exposed to IAV. Passage-2 NHNE cells were inoculated with the IAV WSN/33 for 1, 2, and 3 days to assess the capacity of IFN and the relationship between ROS-generation and IFN-λ secretion, for controlling IAV infection. Viral titer and IAV mRNA level increased after infection. In concert with viral titer, we found that generation of IFNs, such as IFN-?, IFN-λ1 and IFN-λ2/3 was induced after IAV infection until three days post of infection (PI). Induction of IFN-λ-gene expression and protein secretion might be predominant after IAV infection. Similarly, we observed that intracellular ROS generation increased 60 minutes after IAV infection. Viral titer and mRNA level of IAV were significantly higher in cases with scavenging ROS, in cases with an induced IFN-λ mRNA level or where secreted protein concentration of IFN-λ was attenuated after suppression of ROS generation. Both mitochondrial and Duox2-generated ROS were correlated with IAV mRNA and viral titer. Inhibition of mitochondrial ROS generation and knock-down of Duox2 gene expression highly increased IAV viral titer and decreased IFN-λ secretion. Our findings suggest that production of ROS might be responsible for IFN-λ secretion to control IAV infection. Both mitochondria and Duox2 are possible sources of ROS generation, which is required to initiate an innate immune response in NHNE cells.
PMID:
23786562
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23786562