Nox1 oxidase suppresses influenza a virus-induced lung inflammation and oxidative stress
Influenza A virus infection is an ongoing clinical problem and thus, there is an urgent need to understand the mechanisms that regulate the lung inflammation in order to unravel novel generic pharmacological strategies. Evidence indicates that the Nox2-containing NADPH oxidase enzyme promotes influe...
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| Veröffentlicht in: | PloS one 2013-04, Vol.8 (4), p.e60792 |
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| description | Influenza A virus infection is an ongoing clinical problem and thus, there is an urgent need to understand the mechanisms that regulate the lung inflammation in order to unravel novel generic pharmacological strategies. Evidence indicates that the Nox2-containing NADPH oxidase enzyme promotes influenza A virus-induced lung oxidative stress, inflammation and dysfunction via ROS generation. In addition, lung epithelial and endothelial cells express the Nox1 isoform of NADPH oxidase, placing this enzyme at key sites to regulate influenza A virus-induced lung inflammation. The aim of this study was to investigate whether Nox1 oxidase regulates the inflammatory response and the oxidative stress to influenza infection in vivo in mice. Male WT and Nox1-deficient (Nox1(-/y)) mice were infected with the moderately pathogenic HkX-31 (H3N2, 1×10(4) PFU) influenza A virus for analysis of bodyweight, airways inflammation, oxidative stress, viral titre, lung histopathology, and cytokine/chemokine expression at 3 and 7 days post infection. HkX-31 virus infection of Nox1(-/y) mice resulted in significantly greater: loss of bodyweight (Day 3); BALF neutrophilia, peri-bronchial, peri-vascular and alveolar inflammation; Nox2-dependent inflammatory cell ROS production and peri-bronchial, epithelial and endothelial oxidative stress. The expression of pro-inflammatory cytokines including CCL2, CCL3, CXCL2, IL-1β, IL-6, GM-CSF and TNF-α was higher in Nox1(-/y) lungs compared to WT mice at Day 3, however, the expression of CCL2, CCL3, CXCL2, IFN-γ and the anti-inflammatory cytokine IL-10 were lower in lungs of Nox1(-/y) mice vs. WT mice at Day 7. Lung viral titre, and airways infiltration of active CD8(+) and CD4(+) T lymphocytes, and of Tregs were similar between WT and Nox1(-/y) mice. In conclusion, Nox1 oxidase suppresses influenza A virus induced lung inflammation and oxidative stress in mice particularly at the early phases of the infection. Nox1 and Nox2 oxidases appear to have opposing roles in the regulation of inflammation caused by influenza A viruses. |
| doi_str_mv | 10.1371/journal.pone.0060792 |
| format | Article |
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Evidence indicates that the Nox2-containing NADPH oxidase enzyme promotes influenza A virus-induced lung oxidative stress, inflammation and dysfunction via ROS generation. In addition, lung epithelial and endothelial cells express the Nox1 isoform of NADPH oxidase, placing this enzyme at key sites to regulate influenza A virus-induced lung inflammation. The aim of this study was to investigate whether Nox1 oxidase regulates the inflammatory response and the oxidative stress to influenza infection in vivo in mice. Male WT and Nox1-deficient (Nox1(-/y)) mice were infected with the moderately pathogenic HkX-31 (H3N2, 1×10(4) PFU) influenza A virus for analysis of bodyweight, airways inflammation, oxidative stress, viral titre, lung histopathology, and cytokine/chemokine expression at 3 and 7 days post infection. HkX-31 virus infection of Nox1(-/y) mice resulted in significantly greater: loss of bodyweight (Day 3); BALF neutrophilia, peri-bronchial, peri-vascular and alveolar inflammation; Nox2-dependent inflammatory cell ROS production and peri-bronchial, epithelial and endothelial oxidative stress. The expression of pro-inflammatory cytokines including CCL2, CCL3, CXCL2, IL-1β, IL-6, GM-CSF and TNF-α was higher in Nox1(-/y) lungs compared to WT mice at Day 3, however, the expression of CCL2, CCL3, CXCL2, IFN-γ and the anti-inflammatory cytokine IL-10 were lower in lungs of Nox1(-/y) mice vs. WT mice at Day 7. Lung viral titre, and airways infiltration of active CD8(+) and CD4(+) T lymphocytes, and of Tregs were similar between WT and Nox1(-/y) mice. In conclusion, Nox1 oxidase suppresses influenza A virus induced lung inflammation and oxidative stress in mice particularly at the early phases of the infection. Nox1 and Nox2 oxidases appear to have opposing roles in the regulation of inflammation caused by influenza A viruses.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0060792</identifier><identifier>PMID: 23577160</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alveoli ; Analysis ; Animals ; Biology ; Body Weight ; Bronchoalveolar Lavage Fluid - virology ; CCL3 protein ; CD4 antigen ; CD8 antigen ; Chemokines ; Chemokines - metabolism ; CYBB protein ; Cytokines ; Endothelial cells ; Endothelium ; Enzymes ; Gene Deletion ; Gene expression ; Granulocyte-macrophage colony-stimulating factor ; Health aspects ; Histopathology ; Infections ; Infiltration ; Inflammation ; Inflammation - enzymology ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - virology ; Inflammatory response ; Influenza ; Influenza A ; Influenza A virus - physiology ; Interferon ; Interleukin 10 ; Interleukin 6 ; Localization ; Lung - enzymology ; Lung - immunology ; Lung - metabolism ; Lung - virology ; Lungs ; Lymphocytes ; Lymphocytes T ; Male ; Medicine ; Mice ; Mice, Inbred C57BL ; Monocyte chemoattractant protein 1 ; NAD(P)H oxidase ; NADH, NADPH Oxidoreductases - deficiency ; NADH, NADPH Oxidoreductases - genetics ; NADH, NADPH Oxidoreductases - metabolism ; NADPH Oxidase 1 ; Neutrophilia ; Nitric oxide ; Oxidase ; Oxidases ; Oxidative Stress ; Peroxynitrous Acid - biosynthesis ; Peroxynitrous Acid - metabolism ; Pharmacology ; Phenotype ; Rodents ; Superoxides - metabolism ; T-Lymphocyte Subsets - immunology ; Tumor necrosis factor-α ; Viral infections ; Viral Load ; Viruses ; γ-Interferon</subject><ispartof>PloS one, 2013-04, Vol.8 (4), p.e60792</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Selemidis et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Selemidis et al 2013 Selemidis et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-694c2841723103df1eeb71c30507c507ce6bb84e55e30a1ce96d572af678b8523</citedby><cites>FETCH-LOGICAL-c692t-694c2841723103df1eeb71c30507c507ce6bb84e55e30a1ce96d572af678b8523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3620107/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3620107/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23577160$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Selemidis, Stavros</creatorcontrib><creatorcontrib>Seow, Huei Jiunn</creatorcontrib><creatorcontrib>Broughton, Brad R S</creatorcontrib><creatorcontrib>Vinh, Antony</creatorcontrib><creatorcontrib>Bozinovski, Steven</creatorcontrib><creatorcontrib>Sobey, Christopher G</creatorcontrib><creatorcontrib>Drummond, Grant R</creatorcontrib><creatorcontrib>Vlahos, Ross</creatorcontrib><title>Nox1 oxidase suppresses influenza a virus-induced lung inflammation and oxidative stress</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Influenza A virus infection is an ongoing clinical problem and thus, there is an urgent need to understand the mechanisms that regulate the lung inflammation in order to unravel novel generic pharmacological strategies. Evidence indicates that the Nox2-containing NADPH oxidase enzyme promotes influenza A virus-induced lung oxidative stress, inflammation and dysfunction via ROS generation. In addition, lung epithelial and endothelial cells express the Nox1 isoform of NADPH oxidase, placing this enzyme at key sites to regulate influenza A virus-induced lung inflammation. The aim of this study was to investigate whether Nox1 oxidase regulates the inflammatory response and the oxidative stress to influenza infection in vivo in mice. Male WT and Nox1-deficient (Nox1(-/y)) mice were infected with the moderately pathogenic HkX-31 (H3N2, 1×10(4) PFU) influenza A virus for analysis of bodyweight, airways inflammation, oxidative stress, viral titre, lung histopathology, and cytokine/chemokine expression at 3 and 7 days post infection. HkX-31 virus infection of Nox1(-/y) mice resulted in significantly greater: loss of bodyweight (Day 3); BALF neutrophilia, peri-bronchial, peri-vascular and alveolar inflammation; Nox2-dependent inflammatory cell ROS production and peri-bronchial, epithelial and endothelial oxidative stress. The expression of pro-inflammatory cytokines including CCL2, CCL3, CXCL2, IL-1β, IL-6, GM-CSF and TNF-α was higher in Nox1(-/y) lungs compared to WT mice at Day 3, however, the expression of CCL2, CCL3, CXCL2, IFN-γ and the anti-inflammatory cytokine IL-10 were lower in lungs of Nox1(-/y) mice vs. WT mice at Day 7. Lung viral titre, and airways infiltration of active CD8(+) and CD4(+) T lymphocytes, and of Tregs were similar between WT and Nox1(-/y) mice. In conclusion, Nox1 oxidase suppresses influenza A virus induced lung inflammation and oxidative stress in mice particularly at the early phases of the infection. Nox1 and Nox2 oxidases appear to have opposing roles in the regulation of inflammation caused by influenza A viruses.</description><subject>Alveoli</subject><subject>Analysis</subject><subject>Animals</subject><subject>Biology</subject><subject>Body Weight</subject><subject>Bronchoalveolar Lavage Fluid - virology</subject><subject>CCL3 protein</subject><subject>CD4 antigen</subject><subject>CD8 antigen</subject><subject>Chemokines</subject><subject>Chemokines - metabolism</subject><subject>CYBB protein</subject><subject>Cytokines</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Enzymes</subject><subject>Gene Deletion</subject><subject>Gene expression</subject><subject>Granulocyte-macrophage colony-stimulating factor</subject><subject>Health aspects</subject><subject>Histopathology</subject><subject>Infections</subject><subject>Infiltration</subject><subject>Inflammation</subject><subject>Inflammation - enzymology</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - virology</subject><subject>Inflammatory response</subject><subject>Influenza</subject><subject>Influenza A</subject><subject>Influenza A virus - physiology</subject><subject>Interferon</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>Localization</subject><subject>Lung - enzymology</subject><subject>Lung - immunology</subject><subject>Lung - metabolism</subject><subject>Lung - virology</subject><subject>Lungs</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Monocyte chemoattractant protein 1</subject><subject>NAD(P)H oxidase</subject><subject>NADH, NADPH Oxidoreductases - deficiency</subject><subject>NADH, NADPH Oxidoreductases - genetics</subject><subject>NADH, NADPH Oxidoreductases - metabolism</subject><subject>NADPH Oxidase 1</subject><subject>Neutrophilia</subject><subject>Nitric oxide</subject><subject>Oxidase</subject><subject>Oxidases</subject><subject>Oxidative Stress</subject><subject>Peroxynitrous Acid - biosynthesis</subject><subject>Peroxynitrous Acid - metabolism</subject><subject>Pharmacology</subject><subject>Phenotype</subject><subject>Rodents</subject><subject>Superoxides - metabolism</subject><subject>T-Lymphocyte Subsets - immunology</subject><subject>Tumor necrosis factor-α</subject><subject>Viral infections</subject><subject>Viral Load</subject><subject>Viruses</subject><subject>γ-Interferon</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkltr2zAYhs1YWbtu_2BshsFgF8l0sA6-GZSyQ6C0sBO7E7L0OVGwrVSyQ7ZfP6VxSwwbDGNspOd7LF6_WfYCozmmAr9b-yF0uplvfAdzhDgSJXmUneGSkhkniD4-ej_Nnsa4RohRyfmT7JRQJgTm6Cz7ee13OPc7Z3WEPA6bTYAYIeauq5sBut861_nWhSHOXGcHAzZvhm55t63bVvfOd7nu7EHRu22S9HvFs-yk1k2E5-PzPPv-8cO3y8-zq5tPi8uLq5nhJelnvCwMkQUWhGJEbY0BKoENRQwJs7-BV5UsgDGgSGMDJbdMEF1zISvJCD3PXh28m8ZHNYYSFaYUyZIRQhOxOBDW67XaBNfq8Et57dTdgg9LpUPvTAOKUQKM1LXkuijKimtSISlBWmY1qmpIrvfj14aqBWug64NuJtLpTudWaum3iqbfgJFIgtejIPjbAWL_jyOP1FKnU6WsfZKZ1kWjLgohqRQFZYma_4VKl4XWmVSL2qX1ycDbyUBietj1Sz3EqBZfv_w_e_Njyr45Ylegm34VfTPsyxGnYHEATfAxBqgfksNI7Vt9n4bat1qNrU5jL49Tfxi6rzH9A6dt8tk</recordid><startdate>20130408</startdate><enddate>20130408</enddate><creator>Selemidis, Stavros</creator><creator>Seow, Huei Jiunn</creator><creator>Broughton, Brad R S</creator><creator>Vinh, Antony</creator><creator>Bozinovski, Steven</creator><creator>Sobey, Christopher G</creator><creator>Drummond, Grant R</creator><creator>Vlahos, Ross</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130408</creationdate><title>Nox1 oxidase suppresses influenza a virus-induced lung inflammation and oxidative stress</title><author>Selemidis, Stavros ; Seow, Huei Jiunn ; Broughton, Brad R S ; Vinh, Antony ; Bozinovski, Steven ; Sobey, Christopher G ; Drummond, Grant R ; Vlahos, Ross</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-694c2841723103df1eeb71c30507c507ce6bb84e55e30a1ce96d572af678b8523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alveoli</topic><topic>Analysis</topic><topic>Animals</topic><topic>Biology</topic><topic>Body Weight</topic><topic>Bronchoalveolar Lavage Fluid - 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metabolism</topic><topic>Lung - virology</topic><topic>Lungs</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Monocyte chemoattractant protein 1</topic><topic>NAD(P)H oxidase</topic><topic>NADH, NADPH Oxidoreductases - deficiency</topic><topic>NADH, NADPH Oxidoreductases - genetics</topic><topic>NADH, NADPH Oxidoreductases - metabolism</topic><topic>NADPH Oxidase 1</topic><topic>Neutrophilia</topic><topic>Nitric oxide</topic><topic>Oxidase</topic><topic>Oxidases</topic><topic>Oxidative Stress</topic><topic>Peroxynitrous Acid - biosynthesis</topic><topic>Peroxynitrous Acid - metabolism</topic><topic>Pharmacology</topic><topic>Phenotype</topic><topic>Rodents</topic><topic>Superoxides - metabolism</topic><topic>T-Lymphocyte Subsets - immunology</topic><topic>Tumor necrosis factor-α</topic><topic>Viral infections</topic><topic>Viral Load</topic><topic>Viruses</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Selemidis, Stavros</creatorcontrib><creatorcontrib>Seow, Huei Jiunn</creatorcontrib><creatorcontrib>Broughton, Brad R S</creatorcontrib><creatorcontrib>Vinh, Antony</creatorcontrib><creatorcontrib>Bozinovski, Steven</creatorcontrib><creatorcontrib>Sobey, Christopher G</creatorcontrib><creatorcontrib>Drummond, Grant R</creatorcontrib><creatorcontrib>Vlahos, Ross</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Selemidis, Stavros</au><au>Seow, Huei Jiunn</au><au>Broughton, Brad R S</au><au>Vinh, Antony</au><au>Bozinovski, Steven</au><au>Sobey, Christopher G</au><au>Drummond, Grant R</au><au>Vlahos, Ross</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nox1 oxidase suppresses influenza a virus-induced lung inflammation and oxidative stress</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-04-08</date><risdate>2013</risdate><volume>8</volume><issue>4</issue><spage>e60792</spage><pages>e60792-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Influenza A virus infection is an ongoing clinical problem and thus, there is an urgent need to understand the mechanisms that regulate the lung inflammation in order to unravel novel generic pharmacological strategies. Evidence indicates that the Nox2-containing NADPH oxidase enzyme promotes influenza A virus-induced lung oxidative stress, inflammation and dysfunction via ROS generation. In addition, lung epithelial and endothelial cells express the Nox1 isoform of NADPH oxidase, placing this enzyme at key sites to regulate influenza A virus-induced lung inflammation. The aim of this study was to investigate whether Nox1 oxidase regulates the inflammatory response and the oxidative stress to influenza infection in vivo in mice. Male WT and Nox1-deficient (Nox1(-/y)) mice were infected with the moderately pathogenic HkX-31 (H3N2, 1×10(4) PFU) influenza A virus for analysis of bodyweight, airways inflammation, oxidative stress, viral titre, lung histopathology, and cytokine/chemokine expression at 3 and 7 days post infection. HkX-31 virus infection of Nox1(-/y) mice resulted in significantly greater: loss of bodyweight (Day 3); BALF neutrophilia, peri-bronchial, peri-vascular and alveolar inflammation; Nox2-dependent inflammatory cell ROS production and peri-bronchial, epithelial and endothelial oxidative stress. The expression of pro-inflammatory cytokines including CCL2, CCL3, CXCL2, IL-1β, IL-6, GM-CSF and TNF-α was higher in Nox1(-/y) lungs compared to WT mice at Day 3, however, the expression of CCL2, CCL3, CXCL2, IFN-γ and the anti-inflammatory cytokine IL-10 were lower in lungs of Nox1(-/y) mice vs. WT mice at Day 7. Lung viral titre, and airways infiltration of active CD8(+) and CD4(+) T lymphocytes, and of Tregs were similar between WT and Nox1(-/y) mice. In conclusion, Nox1 oxidase suppresses influenza A virus induced lung inflammation and oxidative stress in mice particularly at the early phases of the infection. Nox1 and Nox2 oxidases appear to have opposing roles in the regulation of inflammation caused by influenza A viruses.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23577160</pmid><doi>10.1371/journal.pone.0060792</doi><tpages>e60792</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-04, Vol.8 (4), p.e60792 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1330895223 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Alveoli Analysis Animals Biology Body Weight Bronchoalveolar Lavage Fluid - virology CCL3 protein CD4 antigen CD8 antigen Chemokines Chemokines - metabolism CYBB protein Cytokines Endothelial cells Endothelium Enzymes Gene Deletion Gene expression Granulocyte-macrophage colony-stimulating factor Health aspects Histopathology Infections Infiltration Inflammation Inflammation - enzymology Inflammation - immunology Inflammation - metabolism Inflammation - virology Inflammatory response Influenza Influenza A Influenza A virus - physiology Interferon Interleukin 10 Interleukin 6 Localization Lung - enzymology Lung - immunology Lung - metabolism Lung - virology Lungs Lymphocytes Lymphocytes T Male Medicine Mice Mice, Inbred C57BL Monocyte chemoattractant protein 1 NAD(P)H oxidase NADH, NADPH Oxidoreductases - deficiency NADH, NADPH Oxidoreductases - genetics NADH, NADPH Oxidoreductases - metabolism NADPH Oxidase 1 Neutrophilia Nitric oxide Oxidase Oxidases Oxidative Stress Peroxynitrous Acid - biosynthesis Peroxynitrous Acid - metabolism Pharmacology Phenotype Rodents Superoxides - metabolism T-Lymphocyte Subsets - immunology Tumor necrosis factor-α Viral infections Viral Load Viruses γ-Interferon |
| title | Nox1 oxidase suppresses influenza a virus-induced lung inflammation and oxidative stress |
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