Targeting Evolutionary Conserved Oxidative Stress and Immunometabolic Pathways for the Treatment of Respiratory Infectious Diseases.
Identifieur interne : 000147 ( Main/Exploration ); précédent : 000146; suivant : 000148Targeting Evolutionary Conserved Oxidative Stress and Immunometabolic Pathways for the Treatment of Respiratory Infectious Diseases.
Auteurs : Jonathan R. Erlich [Australie] ; Eunice E. To [Australie] ; Stella Liong [Australie] ; Robert Brooks [Australie] ; Ross Vlahos [Australie] ; John J. O'Leary [Australie] ; Doug A. Brooks [Australie] ; Stavros Selemidis [Australie]Source :
- Antioxidants & redox signaling [ 1557-7716 ] ; 2020.
Abstract
Significance: Up until recently, metabolism has scarcely been referenced in terms of immunology. However, emerging evidence has shown that immune cells undergo an adaptation of metabolic processes, known as the metabolic switch. This switch is key to the activation, and sustained inflammatory phenotype in immune cells, which includes the production of cytokines and reactive oxygen species (ROS) that underpin infectious diseases, respiratory and cardiovascular disease, neurodegenerative disease, as well as cancer. Recent Advances: There is a burgeoning body of evidence that immunometabolism and redox biology drive infectious diseases. For example, influenza A virus (IAV) utilizes endogenous ROS production via NADPH oxidase (NOX)2-containing NOXs and mitochondria to circumvent antiviral responses. These evolutionary conserved processes are promoted by glycolysis, the pentose phosphate pathway, and the tricarboxylic acid (TCA) cycle that drive inflammation. Such metabolic products involve succinate, which stimulates inflammation through ROS-dependent stabilization of hypoxia-inducible factor-1α, promoting interleukin-1β production by the inflammasome. In addition, itaconate has recently gained significant attention for its role as an anti-inflammatory and antioxidant metabolite of the TCA cycle. Critical Issues: The molecular mechanisms by which immunometabolism and ROS promote viral and bacterial pathology are largely unknown. This review will provide an overview of the current paradigms with an emphasis on the roles of immunometabolism and ROS in the context of IAV infection and secondary complications due to bacterial infection such as Streptococcus pneumoniae. Future Directions: Molecular targets based on metabolic cell processes and ROS generation may provide novel and effective therapeutic strategies for IAV and associated bacterial superinfections.
DOI: 10.1089/ars.2020.8028
PubMed: 32008371
Affiliations:
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To</name><affiliation wicri:level="1"><nlm:affiliation>Program in Chronic Infectious and Inflammatory Diseases, Oxidant and Inflammation Biology Group, School of Health and Biomedical Sciences, College of Science, Engineering & Health, RMIT University, Bundoora, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Program in Chronic Infectious and Inflammatory Diseases, Oxidant and Inflammation Biology Group, School of Health and Biomedical Sciences, College of Science, Engineering & Health, RMIT University, Bundoora</wicri:regionArea><wicri:noRegion>Bundoora</wicri:noRegion></affiliation></author><author><name sortKey="Liong, Stella" sort="Liong, Stella" uniqKey="Liong S" first="Stella" last="Liong">Stella Liong</name><affiliation wicri:level="1"><nlm:affiliation>Program in Chronic Infectious and Inflammatory Diseases, Oxidant and Inflammation Biology Group, School of Health and Biomedical Sciences, College of Science, Engineering & Health, RMIT University, Bundoora, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Program in Chronic Infectious and Inflammatory Diseases, Oxidant and Inflammation Biology Group, School of Health and Biomedical Sciences, College of Science, Engineering & Health, RMIT University, Bundoora</wicri:regionArea><wicri:noRegion>Bundoora</wicri:noRegion></affiliation></author><author><name sortKey="Brooks, Robert" sort="Brooks, Robert" uniqKey="Brooks R" first="Robert" last="Brooks">Robert Brooks</name><affiliation wicri:level="1"><nlm:affiliation>School of Pharmacy and Medical Sciences, University of South Australia Cancer Research Institute, University of South Australia, Adelaide, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Pharmacy and Medical Sciences, University of South Australia Cancer Research Institute, University of South Australia, Adelaide</wicri:regionArea><wicri:noRegion>Adelaide</wicri:noRegion></affiliation></author><author><name sortKey="Vlahos, Ross" sort="Vlahos, Ross" uniqKey="Vlahos R" first="Ross" last="Vlahos">Ross Vlahos</name><affiliation wicri:level="1"><nlm:affiliation>Program in Chronic Infectious and Inflammatory Diseases, Oxidant and Inflammation Biology Group, School of Health and Biomedical Sciences, College of Science, Engineering & Health, RMIT University, Bundoora, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Program in Chronic Infectious and Inflammatory Diseases, Oxidant and Inflammation Biology Group, School of Health and Biomedical Sciences, College of Science, Engineering & Health, RMIT University, Bundoora</wicri:regionArea><wicri:noRegion>Bundoora</wicri:noRegion></affiliation></author><author><name sortKey="O Leary, John J" sort="O Leary, John J" uniqKey="O Leary J" first="John J" last="O'Leary">John J. O'Leary</name><affiliation wicri:level="1"><nlm:affiliation>School of Pharmacy and Medical Sciences, University of South Australia Cancer Research Institute, University of South Australia, Adelaide, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Pharmacy and Medical Sciences, University of South Australia Cancer Research Institute, University of South Australia, Adelaide</wicri:regionArea><wicri:noRegion>Adelaide</wicri:noRegion></affiliation></author><author><name sortKey="Brooks, Doug A" sort="Brooks, Doug A" uniqKey="Brooks D" first="Doug A" last="Brooks">Doug A. Brooks</name><affiliation wicri:level="1"><nlm:affiliation>School of Pharmacy and Medical Sciences, University of South Australia Cancer Research Institute, University of South Australia, Adelaide, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Pharmacy and Medical Sciences, University of South Australia Cancer Research Institute, University of South Australia, Adelaide</wicri:regionArea><wicri:noRegion>Adelaide</wicri:noRegion></affiliation></author><author><name sortKey="Selemidis, Stavros" sort="Selemidis, Stavros" uniqKey="Selemidis S" first="Stavros" last="Selemidis">Stavros Selemidis</name><affiliation wicri:level="1"><nlm:affiliation>Program in Chronic Infectious and Inflammatory Diseases, Oxidant and Inflammation Biology Group, School of Health and Biomedical Sciences, College of Science, Engineering & Health, RMIT University, Bundoora, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Program in Chronic Infectious and Inflammatory Diseases, Oxidant and Inflammation Biology Group, School of Health and Biomedical Sciences, College of Science, Engineering & Health, RMIT University, Bundoora</wicri:regionArea><wicri:noRegion>Bundoora</wicri:noRegion></affiliation></author></analytic><series><title level="j">Antioxidants & redox signaling</title><idno type="eISSN">1557-7716</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><b><i>Significance:</i></b> Up until recently, metabolism has scarcely been referenced in terms of immunology. However, emerging evidence has shown that immune cells undergo an adaptation of metabolic processes, known as the metabolic switch. This switch is key to the activation, and sustained inflammatory phenotype in immune cells, which includes the production of cytokines and reactive oxygen species (ROS) that underpin infectious diseases, respiratory and cardiovascular disease, neurodegenerative disease, as well as cancer. <b><i>Recent Advances:</i></b> There is a burgeoning body of evidence that immunometabolism and redox biology drive infectious diseases. For example, influenza A virus (IAV) utilizes endogenous ROS production <i>via</i> NADPH oxidase (NOX)2-containing NOXs and mitochondria to circumvent antiviral responses. These evolutionary conserved processes are promoted by glycolysis, the pentose phosphate pathway, and the tricarboxylic acid (TCA) cycle that drive inflammation. Such metabolic products involve succinate, which stimulates inflammation through ROS-dependent stabilization of hypoxia-inducible factor-1α, promoting interleukin-1β production by the inflammasome. In addition, itaconate has recently gained significant attention for its role as an anti-inflammatory and antioxidant metabolite of the TCA cycle. <b><i>Critical Issues:</i></b> The molecular mechanisms by which immunometabolism and ROS promote viral and bacterial pathology are largely unknown. This review will provide an overview of the current paradigms with an emphasis on the roles of immunometabolism and ROS in the context of IAV infection and secondary complications due to bacterial infection such as <i>Streptococcus pneumoniae</i>. <b><i>Future Directions:</i></b> Molecular targets based on metabolic cell processes and ROS generation may provide novel and effective therapeutic strategies for IAV and associated bacterial superinfections.</div></front></TEI><affiliations><list><country><li>Australie</li></country></list><tree><country name="Australie"><noRegion><name sortKey="Erlich, Jonathan R" sort="Erlich, Jonathan R" uniqKey="Erlich J" first="Jonathan R" last="Erlich">Jonathan R. Erlich</name></noRegion><name sortKey="Brooks, Doug A" sort="Brooks, Doug A" uniqKey="Brooks D" first="Doug A" last="Brooks">Doug A. Brooks</name><name sortKey="Brooks, Robert" sort="Brooks, Robert" uniqKey="Brooks R" first="Robert" last="Brooks">Robert Brooks</name><name sortKey="Liong, Stella" sort="Liong, Stella" uniqKey="Liong S" first="Stella" last="Liong">Stella Liong</name><name sortKey="O Leary, John J" sort="O Leary, John J" uniqKey="O Leary J" first="John J" last="O'Leary">John J. O'Leary</name><name sortKey="Selemidis, Stavros" sort="Selemidis, Stavros" uniqKey="Selemidis S" first="Stavros" last="Selemidis">Stavros Selemidis</name><name sortKey="To, Eunice E" sort="To, Eunice E" uniqKey="To E" first="Eunice E" last="To">Eunice E. To</name><name sortKey="Vlahos, Ross" sort="Vlahos, Ross" uniqKey="Vlahos R" first="Ross" last="Vlahos">Ross Vlahos</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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