Oxidative Stress Enhances Toll-Like Receptor 3 Response to Double-Stranded RNA in Airway Epithelial Cells
Identifieur interne : 000146 ( Ncbi/Merge ); précédent : 000145; suivant : 000147Oxidative Stress Enhances Toll-Like Receptor 3 Response to Double-Stranded RNA in Airway Epithelial Cells
Auteurs : Akira Koarai [Japon] ; Hisatoshi Sugiura [Japon] ; Satoru Yanagisawa [Japon] ; Tomohiro Ichikawa [Japon] ; Yoshiaki Minakata [Japon] ; Kazuto Matsunaga [Japon] ; Tsunahiko Hirano [Japon] ; Keiichiro Akamatsu [Japon] ; Masakazu Ichinose [Japon]Source :
- American Journal of Respiratory Cell and Molecular Biology [ 1044-1549 ] ; 2009.
Abstract
Virus infections are a major cause of chronic obstructive pulmonary disease (COPD) exacerbations. Recently, Toll-like receptor 3 (TLR3) has been demonstrated to react to double-stranded RNA (dsRNA) and to be involved in the immune responses after viral infections. In the present study, we examined whether oxidative stress, which is involved in the pathogenesis of COPD, enhances the responses of TLR3 in airway epithelial cells. The effect of hydrogen peroxide (H2O2) on the release of IL-8 from BEAS-2B cells and primary human bronchial epithelial cells after stimulation with polyinosine-polycytidylic acid [poly(I:C)], a synthetic analog of viral dsRNA and a ligand for TLR3, and the signal transduction were examined. One hundred to 150 μM H2O2 significantly potentiated the release of IL-8 from the epithelial cells after stimulation with 10 μg/ml poly(I:C). The H2O2-augmented IL-8 release was inhibited by treatment with N-acetylcysteine. One hundred micromoles of H2O2 enhanced the translocation of nuclear factor (NF)-κB p65, but not that of interferon regulatory factor-3 (IRF-3), into the nucleus and the NF-κB DNA binding activity after poly(I:C) stimulation, which effect was inhibited not by the silencing of IRF-3 but by MG132, a proteasome inhibitor, or dexamethasone. One hundred micromoles of H2O2 potentiated the TLR3 expression on the airway epithelial cells treated with poly(I:C). These data suggest that oxidative stress augments the response of TLR3 in airway epithelial cells via NF-κB and that this effect might be partly mediated by the enhancement of TLR3 expression. Modulation of this pathway may be a therapeutic target for viral-induced exacerbations of COPD.
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DOI: 10.1165/rcmb.2008-0345OC
PubMed: 19597128
PubMed Central: 2891495
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last="Matsunaga">Kazuto Matsunaga</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Hirano, Tsunahiko" sort="Hirano, Tsunahiko" uniqKey="Hirano T" first="Tsunahiko" last="Hirano">Tsunahiko Hirano</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Akamatsu, Keiichiro" sort="Akamatsu, Keiichiro" uniqKey="Akamatsu K" first="Keiichiro" last="Akamatsu">Keiichiro Akamatsu</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Ichinose, Masakazu" sort="Ichinose, Masakazu" uniqKey="Ichinose M" first="Masakazu" last="Ichinose">Masakazu Ichinose</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, 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Toll-Like Receptor 3 Response to Double-Stranded RNA in Airway Epithelial Cells</title><author><name sortKey="Koarai, Akira" sort="Koarai, Akira" uniqKey="Koarai A" first="Akira" last="Koarai">Akira Koarai</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Sugiura, Hisatoshi" sort="Sugiura, Hisatoshi" uniqKey="Sugiura H" first="Hisatoshi" last="Sugiura">Hisatoshi Sugiura</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Yanagisawa, Satoru" sort="Yanagisawa, Satoru" uniqKey="Yanagisawa S" first="Satoru" last="Yanagisawa">Satoru Yanagisawa</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Ichikawa, Tomohiro" sort="Ichikawa, Tomohiro" uniqKey="Ichikawa T" first="Tomohiro" last="Ichikawa">Tomohiro Ichikawa</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Minakata, Yoshiaki" sort="Minakata, Yoshiaki" uniqKey="Minakata Y" first="Yoshiaki" last="Minakata">Yoshiaki Minakata</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Matsunaga, Kazuto" sort="Matsunaga, Kazuto" uniqKey="Matsunaga K" first="Kazuto" last="Matsunaga">Kazuto Matsunaga</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Hirano, Tsunahiko" sort="Hirano, Tsunahiko" uniqKey="Hirano T" first="Tsunahiko" last="Hirano">Tsunahiko Hirano</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Akamatsu, Keiichiro" sort="Akamatsu, Keiichiro" uniqKey="Akamatsu K" first="Keiichiro" last="Akamatsu">Keiichiro Akamatsu</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author><author><name sortKey="Ichinose, Masakazu" sort="Ichinose, Masakazu" uniqKey="Ichinose M" first="Masakazu" last="Ichinose">Masakazu Ichinose</name><affiliation wicri:level="1"><nlm:aff id="aff1">Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama</wicri:regionArea><wicri:noRegion>Wakayama</wicri:noRegion></affiliation></author></analytic><series><title level="j">American Journal of Respiratory Cell and Molecular Biology</title><idno type="ISSN">1044-1549</idno><idno type="eISSN">1535-4989</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Virus infections are a major cause of chronic obstructive pulmonary disease (COPD) exacerbations. Recently, Toll-like receptor 3 (TLR3) has been demonstrated to react to double-stranded RNA (dsRNA) and to be involved in the immune responses after viral infections. In the present study, we examined whether oxidative stress, which is involved in the pathogenesis of COPD, enhances the responses of TLR3 in airway epithelial cells. The effect of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) on the release of IL-8 from BEAS-2B cells and primary human bronchial epithelial cells after stimulation with polyinosine-polycytidylic acid [poly(I:C)], a synthetic analog of viral dsRNA and a ligand for TLR3, and the signal transduction were examined. One hundred to 150 μM H<sub>2</sub>O<sub>2</sub> significantly potentiated the release of IL-8 from the epithelial cells after stimulation with 10 μg/ml poly(I:C). The H<sub>2</sub>O<sub>2</sub>-augmented IL-8 release was inhibited by treatment with N-acetylcysteine. One hundred micromoles of H<sub>2</sub>O<sub>2</sub> enhanced the translocation of nuclear factor (NF)-κB p65, but not that of interferon regulatory factor-3 (IRF-3), into the nucleus and the NF-κB DNA binding activity after poly(I:C) stimulation, which effect was inhibited not by the silencing of IRF-3 but by MG132, a proteasome inhibitor, or dexamethasone. One hundred micromoles of H<sub>2</sub>O<sub>2</sub> potentiated the TLR3 expression on the airway epithelial cells treated with poly(I:C). These data suggest that oxidative stress augments the response of TLR3 in airway epithelial cells via NF-κB and that this effect might be partly mediated by the enhancement of TLR3 expression. Modulation of this pathway may be a therapeutic target for viral-induced exacerbations of COPD.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Respir Cell Mol Biol</journal-id><journal-id journal-id-type="publisher-id">ajrcmb</journal-id><journal-title-group><journal-title>American Journal of Respiratory Cell and Molecular Biology</journal-title></journal-title-group><issn pub-type="ppub">1044-1549</issn><issn pub-type="epub">1535-4989</issn><publisher><publisher-name>American Thoracic Society</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">19597128</article-id><article-id pub-id-type="pmc">2891495</article-id><article-id pub-id-type="publisher-id">ajrccm426651</article-id><article-id pub-id-type="doi">10.1165/rcmb.2008-0345OC</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Oxidative Stress Enhances Toll-Like Receptor 3 Response to Double-Stranded RNA in Airway Epithelial Cells</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Koarai</surname><given-names>Akira</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Sugiura</surname><given-names>Hisatoshi</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Yanagisawa</surname><given-names>Satoru</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Ichikawa</surname><given-names>Tomohiro</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Minakata</surname><given-names>Yoshiaki</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Matsunaga</surname><given-names>Kazuto</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Hirano</surname><given-names>Tsunahiko</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Akamatsu</surname><given-names>Keiichiro</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Ichinose</surname><given-names>Masakazu</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib></contrib-group><aff id="aff1"><label>1</label>Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, Wakayama, Japan</aff><author-notes><corresp>Correspondence and requests for reprints should be addressed to Masakazu Ichinose, M.D., Ph.D., Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, 811-1 Kimiidera, Wakayama 641-8509, Japan. E-mail: <email>masakazu@wakayama-med.ac.jp</email></corresp></author-notes><pub-date pub-type="ppub"><month>6</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>13</day><month>7</month><year>2009</year></pub-date><volume>42</volume><issue>6</issue><fpage>651</fpage><lpage>660</lpage><history><date date-type="received"><day>7</day><month>9</month><year>2008</year></date><date date-type="accepted"><day>7</day><month>6</month><year>2009</year></date></history><permissions><copyright-statement>Copyright © 2010, American Thoracic Society</copyright-statement><copyright-year>2010</copyright-year></permissions><self-uri xlink:title="pdf" xlink:href="AJRCCM426651.pdf"></self-uri><abstract><p>Virus infections are a major cause of chronic obstructive pulmonary disease (COPD) exacerbations. Recently, Toll-like receptor 3 (TLR3) has been demonstrated to react to double-stranded RNA (dsRNA) and to be involved in the immune responses after viral infections. In the present study, we examined whether oxidative stress, which is involved in the pathogenesis of COPD, enhances the responses of TLR3 in airway epithelial cells. The effect of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) on the release of IL-8 from BEAS-2B cells and primary human bronchial epithelial cells after stimulation with polyinosine-polycytidylic acid [poly(I:C)], a synthetic analog of viral dsRNA and a ligand for TLR3, and the signal transduction were examined. One hundred to 150 μM H<sub>2</sub>O<sub>2</sub> significantly potentiated the release of IL-8 from the epithelial cells after stimulation with 10 μg/ml poly(I:C). The H<sub>2</sub>O<sub>2</sub>-augmented IL-8 release was inhibited by treatment with N-acetylcysteine. One hundred micromoles of H<sub>2</sub>O<sub>2</sub> enhanced the translocation of nuclear factor (NF)-κB p65, but not that of interferon regulatory factor-3 (IRF-3), into the nucleus and the NF-κB DNA binding activity after poly(I:C) stimulation, which effect was inhibited not by the silencing of IRF-3 but by MG132, a proteasome inhibitor, or dexamethasone. One hundred micromoles of H<sub>2</sub>O<sub>2</sub> potentiated the TLR3 expression on the airway epithelial cells treated with poly(I:C). These data suggest that oxidative stress augments the response of TLR3 in airway epithelial cells via NF-κB and that this effect might be partly mediated by the enhancement of TLR3 expression. Modulation of this pathway may be a therapeutic target for viral-induced exacerbations of COPD.</p></abstract><kwd-group><kwd>chronic obstructive pulmonary disease</kwd><kwd>exacerbation</kwd><kwd>hydrogen peroxide</kwd><kwd>nuclear factor-κB</kwd></kwd-group></article-meta><notes><fn-group><fn><p>This article has an online supplement, which is accessible from this issue's table of contents at <ext-link ext-link-type="uri" xlink:href="www.atsjournals.org">www.atsjournals.org</ext-link></p></fn><fn><p>Originally Published in Press as DOI: 10.1165/rcmb.2008-0345OC on July 13, 2009</p></fn><fn><p><bold><italic>Conflict of Interest Statement</italic>:</bold> None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.</p></fn></fn-group></notes></front></pmc><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Koarai, Akira" sort="Koarai, Akira" uniqKey="Koarai A" first="Akira" last="Koarai">Akira Koarai</name></noRegion><name sortKey="Akamatsu, Keiichiro" sort="Akamatsu, Keiichiro" uniqKey="Akamatsu K" first="Keiichiro" last="Akamatsu">Keiichiro Akamatsu</name><name sortKey="Hirano, Tsunahiko" sort="Hirano, Tsunahiko" uniqKey="Hirano T" first="Tsunahiko" last="Hirano">Tsunahiko Hirano</name><name sortKey="Ichikawa, Tomohiro" sort="Ichikawa, Tomohiro" uniqKey="Ichikawa T" first="Tomohiro" last="Ichikawa">Tomohiro Ichikawa</name><name sortKey="Ichinose, Masakazu" sort="Ichinose, Masakazu" uniqKey="Ichinose M" first="Masakazu" last="Ichinose">Masakazu Ichinose</name><name sortKey="Matsunaga, Kazuto" sort="Matsunaga, Kazuto" uniqKey="Matsunaga K" first="Kazuto" last="Matsunaga">Kazuto Matsunaga</name><name sortKey="Minakata, Yoshiaki" sort="Minakata, Yoshiaki" uniqKey="Minakata Y" first="Yoshiaki" last="Minakata">Yoshiaki Minakata</name><name sortKey="Sugiura, Hisatoshi" sort="Sugiura, Hisatoshi" uniqKey="Sugiura H" first="Hisatoshi" last="Sugiura">Hisatoshi Sugiura</name><name sortKey="Yanagisawa, Satoru" sort="Yanagisawa, Satoru" uniqKey="Yanagisawa S" first="Satoru" last="Yanagisawa">Satoru Yanagisawa</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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