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Apocynin inhibits reactive oxygen species (ROS) and downregulates chemokine and cytokine production induced by avian influenza H5N1and H7N9 virus infection

Stambas, John, Lowther, Sue and Ye, Siying 2014, Apocynin inhibits reactive oxygen species (ROS) and downregulates chemokine and cytokine production induced by avian influenza H5N1and H7N9 virus infection, Journal of immunology, vol. 192, no. 1, pp. 1-1.


Title Apocynin inhibits reactive oxygen species (ROS) and downregulates chemokine and cytokine production induced by avian influenza H5N1and H7N9 virus infection
Author(s) Stambas, JohnORCID iD for Stambas, John orcid.org/0000-0002-5690-2551
Lowther, Sue
Ye, Siying
Journal name Journal of immunology
Volume number 192
Issue number 1
Article ID Supplement 187.6
Start page 1
End page 1
Total pages 1
Publisher American Association of Immunologists
Place of publication Bethesda, Md.
Publication date 2014-05-01
ISSN 0022-1767
1550-6606
Keyword(s) Science & Technology
Life Sciences & Biomedicine
Immunology
Summary Influenza A virus infection causes acute inflammation resulting in increased reactive oxygen species (ROS) production and lung injury. ROS are produced following activation of the NADPH oxidase enzyme complex. Apocynin, an inhibitor of NADPH oxidase complex formation has been shown to reduce the accumulation of inflammatory cells in the lungs of influenza-infected mice. As hypercytokinemia is thought to contribute to severe disease pathogenesis of both H5N1 and H7N9 infection in humans, we hypothesized that apocynin could reduce virus-induced cytokine/chemokine production. Human lung epithelial and chicken cell lines were infected with low pathogenic avian influenza H7N9 (A/Anhui/1/2013) and HPAI H5N1 (A/chicken/Vietnam/0008/2004) viruses in the absence or presence of apocynin. Quantitative real-time PCR demonstrated that apocynin inhibited influenza-induced cytokines/chemokines and ROS production following infection. Interestingly, addition of apocynin to in vitro cultures significantly increased SOCS1 and SOCS3 mRNA and protein expression, contributing to the negative regulation of overall cytokine expression. We suggest that intervention strategies targeting both the virus (current therapeutics) and the host e.g. apocynin (future therapeutics) could be used to ameliorate disease in infected individuals, reducing hypercytokinemia and pathology and allowing full development of adaptive immune responses.
Language eng
Field of Research 110799 Immunology not elsewhere classified
1107 Immunology
Socio Economic Objective 920109 Infectious Diseases
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2014, American Association of Immunology
Persistent URL http://hdl.handle.net/10536/DRO/DU:30088092

Document type: Journal Article
Collection: School of Medicine
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