Anti-high mobility group box-1 monoclonal antibody treatment provides protection against influenza A virus (H1N1)-induced pneumonia in mice
Identifieur interne : 000233 ( Pmc/Curation ); précédent : 000232; suivant : 000234Anti-high mobility group box-1 monoclonal antibody treatment provides protection against influenza A virus (H1N1)-induced pneumonia in mice
Auteurs : Nobuyuki Nosaka [Japon] ; Masato Yashiro [Japon] ; Mutsuko Yamada [Japon] ; Yosuke Fujii [Japon] ; Hirokazu Tsukahara [Japon] ; Keyue Liu [Japon] ; Masahiro Nishibori [Japon] ; Akihiro Matsukawa [Japon] ; Tsuneo Morishima [Japon]Source :
- Critical Care [ 1364-8535 ] ; 2015.
Abstract
Provision for the emergence of an influenza pandemic is an urgent issue. The discovery of a novel anti-influenza therapeutic approach would increase the effectiveness of traditional virus-based strategies. This study was undertaken to evaluate the therapeutic effects of anti-high mobility group box-1 (HMGB1) monoclonal antibody (mAb) treatment on influenza A virus (H1N1)-induced pneumonia in mice.
Nine-week-old male C57BL/6 mice were inoculated with H1N1, then anti-HMGB1 mAb or control mAb were administered intravenously at 1, 24 and 48 hours after H1N1 inoculation and the survival rate was analyzed. Lung lavage and histopathological analysis were performed on days 3, 5, 7 and 10 after inoculation.
Anti-HMGB1 mAb significantly improved the survival rate of H1N1-inoculated mice (1 out of 15 versus 8 out of 15 deaths in the anti-HMGB1 mAb-treated group versus the control mAb-treated group,
Anti-HMGB1 mAb may provide a novel and effective pharmacological strategy for severe influenza virus infection in humans by reducing the inflammatory responses induced by HMGB1.
The online version of this article (doi:10.1186/s13054-015-0983-9) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s13054-015-0983-9
PubMed: 26067826
PubMed Central: 4490661
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Matsukawa</name><affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="GRID">grid.261356.5</institution-id><institution-id institution-id-type="ISNI">0000000113024472</institution-id><institution>Department of Pathology and Experimental Medicine,</institution><institution>Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,</institution></institution-wrap>Okayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Okayama</wicri:regionArea></affiliation></author><author><name sortKey="Morishima, Tsuneo" sort="Morishima, Tsuneo" uniqKey="Morishima T" first="Tsuneo" last="Morishima">Tsuneo Morishima</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.261356.5</institution-id><institution-id institution-id-type="ISNI">0000000113024472</institution-id><institution>Department of Pediatrics,</institution><institution>Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,</institution></institution-wrap>Okayama, Japan</nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Okayama</wicri:regionArea></affiliation></author></analytic><series><title level="j">Critical Care</title><idno type="ISSN">1364-8535</idno><idno type="eISSN">1466-609X</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Introduction</title><p id="Par1">Provision for the emergence of an influenza pandemic is an urgent issue. The discovery of a novel anti-influenza therapeutic approach would increase the effectiveness of traditional virus-based strategies. This study was undertaken to evaluate the therapeutic effects of anti-high mobility group box-1 (HMGB1) monoclonal antibody (mAb) treatment on influenza A virus (H1N1)-induced pneumonia in mice.</p></sec><sec><title>Methods</title><p id="Par2">Nine-week-old male C57BL/6 mice were inoculated with H1N1, then anti-HMGB1 mAb or control mAb were administered intravenously at 1, 24 and 48 hours after H1N1 inoculation and the survival rate was analyzed. Lung lavage and histopathological analysis were performed on days 3, 5, 7 and 10 after inoculation.</p></sec><sec><title>Results</title><p id="Par3">Anti-HMGB1 mAb significantly improved the survival rate of H1N1-inoculated mice (1 out of 15 versus 8 out of 15 deaths in the anti-HMGB1 mAb-treated group versus the control mAb-treated group, <italic>p</italic> < 0.01), although the treatment did not affect virus propagation in the lungs. The treatment also significantly attenuated histological changes and neutrophil infiltration in the lungs of H1N1-inoculated mice. This was associated with inhibition of HMGB1 and suppression of inflammatory cytokine/chemokine expression and oxidative stress enhancement, which were observed in H1N1-inoculated mice. The expression of receptor for advanced glycation end products and nuclear factor κB was attenuated by the treatment.</p></sec><sec><title>Conclusions</title><p id="Par4">Anti-HMGB1 mAb may provide a novel and effective pharmacological strategy for severe influenza virus infection in humans by reducing the inflammatory responses induced by HMGB1.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (doi:10.1186/s13054-015-0983-9) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Fineberg, Hv" uniqKey="Fineberg H">HV Fineberg</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kumar, A" uniqKey="Kumar A">A Kumar</name></author><author><name sortKey="Zarychanski, R" uniqKey="Zarychanski R">R Zarychanski</name></author><author><name sortKey="Pinto, R" uniqKey="Pinto R">R 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Crit Care</journal-id><journal-title-group><journal-title>Critical Care</journal-title></journal-title-group><issn pub-type="ppub">1364-8535</issn><issn pub-type="epub">1466-609X</issn><publisher><publisher-name>BioMed Central</publisher-name><publisher-loc>London</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26067826</article-id><article-id pub-id-type="pmc">4490661</article-id><article-id pub-id-type="publisher-id">983</article-id><article-id pub-id-type="doi">10.1186/s13054-015-0983-9</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research</subject></subj-group></article-categories><title-group><article-title>Anti-high mobility group box-1 monoclonal antibody treatment provides protection against influenza A virus (H1N1)-induced pneumonia in mice</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Nosaka</surname><given-names>Nobuyuki</given-names></name><address><phone>+81-86-235-7249</phone><email>pv702xz5@s.okayama-u.ac.jp</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Yashiro</surname><given-names>Masato</given-names></name><address><email>yashiro@md.okayama-u.ac.jp</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Yamada</surname><given-names>Mutsuko</given-names></name><address><email>prqv5jku@s.okayama-u.ac.jp</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Fujii</surname><given-names>Yosuke</given-names></name><address><email>fujii-y@cc.okayama-u.ac.jp</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Tsukahara</surname><given-names>Hirokazu</given-names></name><address><email>tsukah-h@cc.okayama-u.ac.jp</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Keyue</given-names></name><address><email>liukeyue@md.okayama-u.ac.jp</email></address><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Nishibori</surname><given-names>Masahiro</given-names></name><address><email>mbori@md.okayama-u.ac.jp</email></address><xref ref-type="aff" rid="Aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Matsukawa</surname><given-names>Akihiro</given-names></name><address><email>amatsu@md.okayama-u.ac.jp</email></address><xref ref-type="aff" rid="Aff3">3</xref></contrib><contrib contrib-type="author"><name><surname>Morishima</surname><given-names>Tsuneo</given-names></name><address><email>tmorishima@okayamah.rofuku.go.jp</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><aff id="Aff1"><label>1</label><institution-wrap><institution-id institution-id-type="GRID">grid.261356.5</institution-id><institution-id institution-id-type="ISNI">0000000113024472</institution-id><institution>Department of Pediatrics,</institution><institution>Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,</institution></institution-wrap>Okayama, Japan</aff><aff id="Aff2"><label>2</label><institution-wrap><institution-id institution-id-type="GRID">grid.261356.5</institution-id><institution-id institution-id-type="ISNI">0000000113024472</institution-id><institution>Department of Pharmacology,</institution><institution>Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,</institution></institution-wrap>Okayama, Japan</aff><aff id="Aff3"><label>3</label><institution-wrap><institution-id institution-id-type="GRID">grid.261356.5</institution-id><institution-id institution-id-type="ISNI">0000000113024472</institution-id><institution>Department of Pathology and Experimental Medicine,</institution><institution>Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,</institution></institution-wrap>Okayama, Japan</aff></contrib-group><pub-date pub-type="epub"><day>11</day><month>6</month><year>2015</year></pub-date><pub-date pub-type="pmc-release"><day>11</day><month>6</month><year>2015</year></pub-date><pub-date pub-type="collection"><year>2015</year></pub-date><volume>19</volume><elocation-id>249</elocation-id><history><date date-type="received"><day>8</day><month>4</month><year>2015</year></date><date date-type="accepted"><day>8</day><month>6</month><year>2015</year></date></history><permissions><copyright-statement>© Nosaka et al. 2015</copyright-statement><license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p></license></permissions><abstract id="Abs1"><sec><title>Introduction</title><p id="Par1">Provision for the emergence of an influenza pandemic is an urgent issue. The discovery of a novel anti-influenza therapeutic approach would increase the effectiveness of traditional virus-based strategies. This study was undertaken to evaluate the therapeutic effects of anti-high mobility group box-1 (HMGB1) monoclonal antibody (mAb) treatment on influenza A virus (H1N1)-induced pneumonia in mice.</p></sec><sec><title>Methods</title><p id="Par2">Nine-week-old male C57BL/6 mice were inoculated with H1N1, then anti-HMGB1 mAb or control mAb were administered intravenously at 1, 24 and 48 hours after H1N1 inoculation and the survival rate was analyzed. Lung lavage and histopathological analysis were performed on days 3, 5, 7 and 10 after inoculation.</p></sec><sec><title>Results</title><p id="Par3">Anti-HMGB1 mAb significantly improved the survival rate of H1N1-inoculated mice (1 out of 15 versus 8 out of 15 deaths in the anti-HMGB1 mAb-treated group versus the control mAb-treated group, <italic>p</italic> < 0.01), although the treatment did not affect virus propagation in the lungs. The treatment also significantly attenuated histological changes and neutrophil infiltration in the lungs of H1N1-inoculated mice. This was associated with inhibition of HMGB1 and suppression of inflammatory cytokine/chemokine expression and oxidative stress enhancement, which were observed in H1N1-inoculated mice. The expression of receptor for advanced glycation end products and nuclear factor κB was attenuated by the treatment.</p></sec><sec><title>Conclusions</title><p id="Par4">Anti-HMGB1 mAb may provide a novel and effective pharmacological strategy for severe influenza virus infection in humans by reducing the inflammatory responses induced by HMGB1.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (doi:10.1186/s13054-015-0983-9) contains supplementary material, which is available to authorized users.</p></sec></abstract><kwd-group xml:lang="en"><title>Keywords</title><kwd>Influenza</kwd><kwd>Influenza Infection</kwd><kwd>Ethyl Pyruvate</kwd><kwd>Virus Inoculation</kwd><kwd>Lung Injury Score</kwd></kwd-group><funding-group><award-group><funding-source><institution>the Japanese Ministry of Health, Labour and Welfare</institution></funding-source><award-id>H24-Shinko-Ippan-002</award-id><principal-award-recipient><name><surname>Morishima</surname><given-names>Tsuneo</given-names></name></principal-award-recipient></award-group></funding-group><funding-group><award-group><funding-source><institution>the Japanese Ministry of Education, Culture, Sports, Science and Technology</institution></funding-source><award-id>25670465</award-id><principal-award-recipient><name><surname>Morishima</surname><given-names>Tsuneo</given-names></name></principal-award-recipient></award-group></funding-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© The Author(s) 2015</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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