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Inhibition of reactive oxygen species production ameliorates inflammation induced by influenza A viruses via upregulation of SOCS1 and SOCS3.

Ye,S, Lowther,S and Stambas,J 2015, Inhibition of reactive oxygen species production ameliorates inflammation induced by influenza A viruses via upregulation of SOCS1 and SOCS3., Journal of Virology, vol. 89, no. 5, pp. 2672-2683, doi: 10.1128/JVI.03529-14.

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Title Inhibition of reactive oxygen species production ameliorates inflammation induced by influenza A viruses via upregulation of SOCS1 and SOCS3.
Author(s) Ye,S
Lowther,S
Stambas,JORCID iD for Stambas,J orcid.org/0000-0002-5690-2551
Journal name Journal of Virology
Volume number 89
Issue number 5
Start page 2672
End page 2683
Total pages o
Publisher American Society for Microbiology
Place of publication United States
Publication date 2015-03
ISSN 1098-5514
1098-5514
Keyword(s) Science & Technology
Life Sciences & Biomedicine
Virology
INNATE IMMUNE-RESPONSES
TAM RECEPTORS
H7N9 VIRUS
EPITHELIAL-CELLS
GENE-EXPRESSION
NADPH OXIDASES
INFECTION
CYTOKINES
FERRETS
PATHWAY
Summary Highly pathogenic avian influenza virus infection is associated with severe mortality in both humans and poultry. The mechanisms of disease pathogenesis and immunity are poorly understood although recent evidence suggests that cytokine/chemokine dysregulation contributes to disease severity following H5N1 infection. Influenza A virus infection causes a rapid influx of inflammatory cells, resulting in increased reactive oxygen species production, cytokine expression, and acute lung injury. Proinflammatory stimuli are known to induce intracellular reactive oxygen species by activating NADPH oxidase activity. We therefore hypothesized that inhibition of this activity would restore host cytokine homeostasis following avian influenza virus infection. A panel of airway epithelial and immune cells from mammalian and avian species were infected with A/Puerto Rico/8/1934 H1N1 virus, low-pathogenicity avian influenza H5N3 virus (A/duck/Victoria/0305-2/2012), highly pathogenic avian influenza H5N1 virus (A/chicken/Vietnam/0008/2004), or low-pathogenicity avian influenza H7N9 virus (A/Anhui/1/2013). Quantitative real-time reverse transcriptase PCR showed that H5N1 and H7N9 viruses significantly stimulated cytokine (interleukin-6, beta interferon, CXCL10, and CCL5) production. Among the influenza-induced cytokines, CCL5 was identified as a potential marker for overactive immunity. Apocynin, a Nox2 inhibitor, inhibited influenza-induced cytokines and reactive oxygen species production, although viral replication was not significantly altered in vitro. Interestingly, apocynin treatment significantly increased influenza virus-induced mRNA and protein expression of SOCS1 and SOCS3, enhancing negative regulation of cytokine signaling. These findings suggest that apocynin or its derivatives (targeting host responses) could be used in combination with antiviral strategies (targeting viruses) as therapeutic agents to ameliorate disease severity in susceptible species.
Language eng
DOI 10.1128/JVI.03529-14
Field of Research 110804 Medical Virology
Socio Economic Objective 920109 Infectious Diseases
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2014, American Society for Microbiology
Persistent URL http://hdl.handle.net/10536/DRO/DU:30070553

Document type: Journal Article
Collection: School of Medicine
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