tetano
Editor, Senior Moderator
J Biol Chem. 2016 Jun 15. pii: jbc.M115.693101. [Epub ahead of print]
[h=1]Gene expression and antiviral activity of interleukin-35 in response to influenza A virus infection.[/h] Wang L[SUP]1[/SUP], Zhu S[SUP]1[/SUP], Xu G[SUP]1[/SUP], Feng J[SUP]1[/SUP], Han T[SUP]1[/SUP], Zhao F[SUP]1[/SUP], She YL[SUP]1[/SUP], Liu S[SUP]1[/SUP], Ye L[SUP]1[/SUP], Zhu Y[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Interleukin (IL)-35 is a newly described member of the IL-12 family. It has been reported to inhibit inflammation and autoimmune inflammatory disease, and can increase apoptotic sensitivity. Little is known about the role of IL-35 during viral infection. Herein, high levels of IL-35 were found in peripheral blood mononuclear cells and throat swabs from patients with seasonal influenza A virus (IAV) relative to healthy individuals. IAV infection of human lung epithelial and primary cells increased levels of IL-35 mRNA and protein. Further studies demonstrated that IAV-induced IL-35 transcription is regulated by NF-kB. IL-35 expression was significantly suppressed by selective inhibitors of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), indicating their involvement in IL-35 expression. Interestingly, IL-35 production may have suppressed IAV RNA replication and viral protein synthesis via induction of type I and III interferons (IFN), leading to activation of downstream IFN effectors, PKR,OAS, and Mx. IL-35 exhibited extensive antiviral activity against the hepatitis B virus, enterovirus 71, and vesicular stomatitis virus. Our results demonstrate that IL-35 is a novel IAV-inducible cytokine, and its production elicits antiviral activity.
Copyright ? 2016, The American Society for Biochemistry and Molecular Biology.
[h=4]KEYWORDS:[/h] NF-kappa B (NF-KB); antiviral agent; host defense; host-pathogen interaction; influenza virus; innate immunity; interferon; interleukin; viral infection
PMID: 27307042 [PubMed - as supplied by publisher] Free full text
[h=1]Gene expression and antiviral activity of interleukin-35 in response to influenza A virus infection.[/h] Wang L[SUP]1[/SUP], Zhu S[SUP]1[/SUP], Xu G[SUP]1[/SUP], Feng J[SUP]1[/SUP], Han T[SUP]1[/SUP], Zhao F[SUP]1[/SUP], She YL[SUP]1[/SUP], Liu S[SUP]1[/SUP], Ye L[SUP]1[/SUP], Zhu Y[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Interleukin (IL)-35 is a newly described member of the IL-12 family. It has been reported to inhibit inflammation and autoimmune inflammatory disease, and can increase apoptotic sensitivity. Little is known about the role of IL-35 during viral infection. Herein, high levels of IL-35 were found in peripheral blood mononuclear cells and throat swabs from patients with seasonal influenza A virus (IAV) relative to healthy individuals. IAV infection of human lung epithelial and primary cells increased levels of IL-35 mRNA and protein. Further studies demonstrated that IAV-induced IL-35 transcription is regulated by NF-kB. IL-35 expression was significantly suppressed by selective inhibitors of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), indicating their involvement in IL-35 expression. Interestingly, IL-35 production may have suppressed IAV RNA replication and viral protein synthesis via induction of type I and III interferons (IFN), leading to activation of downstream IFN effectors, PKR,OAS, and Mx. IL-35 exhibited extensive antiviral activity against the hepatitis B virus, enterovirus 71, and vesicular stomatitis virus. Our results demonstrate that IL-35 is a novel IAV-inducible cytokine, and its production elicits antiviral activity.
Copyright ? 2016, The American Society for Biochemistry and Molecular Biology.
[h=4]KEYWORDS:[/h] NF-kappa B (NF-KB); antiviral agent; host defense; host-pathogen interaction; influenza virus; innate immunity; interferon; interleukin; viral infection
PMID: 27307042 [PubMed - as supplied by publisher] Free full text