Transient receptor potential melastatin 2–mediated heme oxygenase-1 has a role for bacterial clearance by regulating autophagy in peritoneal macrophages during polymicrobial sepsis
Identifieur interne : 000A35 ( Ncbi/Merge ); précédent : 000A34; suivant : 000A36Transient receptor potential melastatin 2–mediated heme oxygenase-1 has a role for bacterial clearance by regulating autophagy in peritoneal macrophages during polymicrobial sepsis
Auteurs : Xiaowei Qian [République populaire de Chine] ; Hao Cheng [République populaire de Chine] ; Xinzhong Chen [République populaire de Chine]Source :
- Innate Immunity [ 1753-4259 ] ; 2019.
Abstract
Our previous study indicated an important protective role of transient receptor potential melastatin 2 (TRPM2) in controlling bacterial clearance in macrophages during polymicrobial sepsis by regulating heme oxygenase-1. Autophagy is necessary for macrophages to kill invasive bacteria. In the present study, TRPM2 knockout (KO) mice show decreased heme oxygenase-1 and autophagy in peritoneal macrophages after caecal ligation and puncture surgery. Caecal ligation and puncture-induced autophagy in peritoneal macrophages is dependent on heme oxygenase-1. TRPM2 KO mice treated with heme oxygenase-1 inducer before caecal ligation and puncture significantly increase autophagy of peritoneal macrophages, bacterial clearance rate and survival rate. In addition, TRPM2 KO mice treated with heme oxygenase-1 inducer before caecal ligation and puncture significantly attenuate organ injury and systemic inflammation. These improvements are reversed by autophagy inhibitor. Therefore, our findings suggest that TRPM2-mediated heme oxygenase-1 has a role for bacterial clearance possibly by regulating autophagy in peritoneal macrophages during polymicrobial sepsis.
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DOI: 10.1177/1753425919875796
PubMed: 31533549
PubMed Central: 6900664
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has a role for bacterial clearance by regulating autophagy in peritoneal
macrophages during polymicrobial sepsis</title><author><name sortKey="Qian, Xiaowei" sort="Qian, Xiaowei" uniqKey="Qian X" first="Xiaowei" last="Qian">Xiaowei Qian</name><affiliation wicri:level="1"><nlm:aff id="aff1-1753425919875796">Department of Anaesthesia, Women’s Hospital, Zhejiang University School of Medicine, PR China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anaesthesia, Women’s Hospital, Zhejiang University School of Medicine</wicri:regionArea><wicri:noRegion>Zhejiang University School of Medicine</wicri:noRegion></affiliation></author><author><name sortKey="Cheng, Hao" sort="Cheng, Hao" uniqKey="Cheng H" first="Hao" last="Cheng">Hao Cheng</name><affiliation wicri:level="1"><nlm:aff id="aff1-1753425919875796">Department of Anaesthesia, Women’s Hospital, Zhejiang University School of Medicine, PR China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anaesthesia, Women’s Hospital, Zhejiang University School of Medicine</wicri:regionArea><wicri:noRegion>Zhejiang University School of Medicine</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2-1753425919875796">Department of Anaesthesia, Lishui Municipal Central Hospital, PR China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anaesthesia, Lishui Municipal Central Hospital</wicri:regionArea><wicri:noRegion>Lishui Municipal Central Hospital</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Xinzhong" sort="Chen, Xinzhong" uniqKey="Chen X" first="Xinzhong" last="Chen">Xinzhong Chen</name><affiliation wicri:level="1"><nlm:aff id="aff1-1753425919875796">Department of Anaesthesia, Women’s Hospital, Zhejiang University School of Medicine, PR China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anaesthesia, Women’s Hospital, Zhejiang University School of Medicine</wicri:regionArea><wicri:noRegion>Zhejiang University School of Medicine</wicri:noRegion></affiliation></author></analytic><series><title level="j">Innate Immunity</title><idno type="ISSN">1753-4259</idno><idno type="eISSN">1753-4267</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Our previous study indicated an important protective role of transient receptor
potential melastatin 2 (TRPM2) in controlling bacterial clearance in macrophages
during polymicrobial sepsis by regulating heme oxygenase-1. Autophagy is
necessary for macrophages to kill invasive bacteria. In the present study, TRPM2
knockout (KO) mice show decreased heme oxygenase-1 and autophagy in peritoneal
macrophages after caecal ligation and puncture surgery. Caecal ligation and
puncture-induced autophagy in peritoneal macrophages is dependent on heme
oxygenase-1. TRPM2 KO mice treated with heme oxygenase-1 inducer before caecal
ligation and puncture significantly increase autophagy of peritoneal
macrophages, bacterial clearance rate and survival rate. In addition, TRPM2 KO
mice treated with heme oxygenase-1 inducer before caecal ligation and puncture
significantly attenuate organ injury and systemic inflammation. These
improvements are reversed by autophagy inhibitor. Therefore, our findings
suggest that TRPM2-mediated heme oxygenase-1 has a role for bacterial clearance
possibly by regulating autophagy in peritoneal macrophages during polymicrobial
sepsis.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Singer, M" uniqKey="Singer M">M Singer</name></author><author><name sortKey="Deutschman, Cs" uniqKey="Deutschman C">CS Deutschman</name></author><author><name sortKey="Seymour, Cw" uniqKey="Seymour C">CW Seymour</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vincent, Jl" uniqKey="Vincent J">JL Vincent</name></author><author><name sortKey="Nelson, Dr" uniqKey="Nelson D">DR Nelson</name></author><author><name sortKey="Williams, Md" uniqKey="Williams M">MD. Williams</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hotchkiss, Rs" uniqKey="Hotchkiss R">RS Hotchkiss</name></author><author><name sortKey="Karl, Ie" uniqKey="Karl I">IE. Karl</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Clapham, De" uniqKey="Clapham D">DE. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Innate Immun</journal-id><journal-id journal-id-type="iso-abbrev">Innate Immun</journal-id><journal-id journal-id-type="publisher-id">INI</journal-id><journal-id journal-id-type="hwp">spini</journal-id><journal-title-group><journal-title>Innate Immunity</journal-title></journal-title-group><issn pub-type="ppub">1753-4259</issn><issn pub-type="epub">1753-4267</issn><publisher><publisher-name>SAGE Publications</publisher-name><publisher-loc>Sage UK: London, England</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31533549</article-id><article-id pub-id-type="pmc">6900664</article-id><article-id pub-id-type="doi">10.1177/1753425919875796</article-id><article-id pub-id-type="publisher-id">10.1177_1753425919875796</article-id><article-categories><subj-group subj-group-type="heading"><subject>Original Articles</subject></subj-group></article-categories><title-group><article-title>Transient receptor potential melastatin 2–mediated heme oxygenase-1
has a role for bacterial clearance by regulating autophagy in peritoneal
macrophages during polymicrobial sepsis</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-9553-1098</contrib-id><name><surname>Qian</surname><given-names>XiaoWei</given-names></name><xref ref-type="aff" rid="aff1-1753425919875796">1</xref></contrib><contrib contrib-type="author"><name><surname>Cheng</surname><given-names>Hao</given-names></name><xref ref-type="aff" rid="aff1-1753425919875796">1</xref><xref ref-type="aff" rid="aff2-1753425919875796">2</xref></contrib><contrib contrib-type="author"><name><surname>Chen</surname><given-names>XinZhong</given-names></name><xref ref-type="aff" rid="aff1-1753425919875796">1</xref><xref ref-type="corresp" rid="corresp1-1753425919875796"></xref></contrib><aff id="aff1-1753425919875796"><label>1</label>Department of Anaesthesia, Women’s Hospital, Zhejiang University School of Medicine, PR China</aff><aff id="aff2-1753425919875796"><label>2</label>Department of Anaesthesia, Lishui Municipal Central Hospital, PR China</aff></contrib-group><author-notes><corresp id="corresp1-1753425919875796">XinZhong Chen, Department of Anaesthesia,
Women’s Hospital, Zhejiang University School of Medicine, Xueshi Road 1,
Hangzhou 310006, PR China. Email: <email>chenxinz@zju.edu.cn</email></corresp></author-notes><pub-date pub-type="epub"><day>19</day><month>9</month><year>2019</year></pub-date><pub-date pub-type="ppub"><month>11</month><year>2019</year></pub-date><volume>25</volume><issue>8</issue><fpage>530</fpage><lpage>538</lpage><history><date date-type="received"><day>3</day><month>4</month><year>2019</year></date><date date-type="accepted"><day>21</day><month>8</month><year>2019</year></date></history><permissions><copyright-statement>© The Author(s) 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder content-type="society">SAGE Publications Ltd unless otherwise
noted. Manuscript content on this site is licensed under Creative Commons
Licenses</copyright-holder><license license-type="creative-commons" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/"><license-p>Creative Commons Non Commercial CC BY-NC: This article is distributed
under the terms of the Creative Commons Attribution-NonCommercial 4.0
License (<ext-link ext-link-type="uri" xlink:href="http://www.creativecommons.org/licenses/by-nc/4.0/">http://www.creativecommons.org/licenses/by-nc/4.0/</ext-link>) which
permits non-commercial use, reproduction and distribution of the work
without further permission provided the original work is attributed as
specified on the SAGE and Open Access pages (<ext-link ext-link-type="uri" xlink:href="https://us.sagepub.com/en-us/nam/open-access-at-sage">https://us.sagepub.com/en-us/nam/open-access-at-sage</ext-link>).</license-p></license></permissions><abstract abstract-type="short"><p>Our previous study indicated an important protective role of transient receptor
potential melastatin 2 (TRPM2) in controlling bacterial clearance in macrophages
during polymicrobial sepsis by regulating heme oxygenase-1. Autophagy is
necessary for macrophages to kill invasive bacteria. In the present study, TRPM2
knockout (KO) mice show decreased heme oxygenase-1 and autophagy in peritoneal
macrophages after caecal ligation and puncture surgery. Caecal ligation and
puncture-induced autophagy in peritoneal macrophages is dependent on heme
oxygenase-1. TRPM2 KO mice treated with heme oxygenase-1 inducer before caecal
ligation and puncture significantly increase autophagy of peritoneal
macrophages, bacterial clearance rate and survival rate. In addition, TRPM2 KO
mice treated with heme oxygenase-1 inducer before caecal ligation and puncture
significantly attenuate organ injury and systemic inflammation. These
improvements are reversed by autophagy inhibitor. Therefore, our findings
suggest that TRPM2-mediated heme oxygenase-1 has a role for bacterial clearance
possibly by regulating autophagy in peritoneal macrophages during polymicrobial
sepsis.</p></abstract><kwd-group><kwd>Transient receptor potential melastatin 2</kwd><kwd>heme oxygenase-1</kwd><kwd>autophagy</kwd><kwd>macrophage</kwd><kwd>sepsis</kwd></kwd-group><funding-group><award-group id="award1-1753425919875796"><funding-source id="funding1-1753425919875796"><institution-wrap><institution>National Natural Science Foundation of China</institution><institution-id institution-id-type="FundRef">http://doi.org/10.13039/501100001809</institution-id></institution-wrap></funding-source><award-id rid="funding1-1753425919875796">81501702</award-id></award-group><award-group id="award2-1753425919875796"><funding-source id="funding2-1753425919875796"><institution-wrap><institution>Natural Science Foundation of Zhejiang
Province</institution><institution-id institution-id-type="FundRef">http://doi.org/10.13039/501100004731</institution-id></institution-wrap></funding-source><award-id rid="funding2-1753425919875796">LY15H150007</award-id></award-group></funding-group></article-meta></front></pmc><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Qian, Xiaowei" sort="Qian, Xiaowei" uniqKey="Qian X" first="Xiaowei" last="Qian">Xiaowei Qian</name></noRegion><name sortKey="Chen, Xinzhong" sort="Chen, Xinzhong" uniqKey="Chen X" first="Xinzhong" last="Chen">Xinzhong Chen</name><name sortKey="Cheng, Hao" sort="Cheng, Hao" uniqKey="Cheng H" first="Hao" last="Cheng">Hao Cheng</name><name sortKey="Cheng, Hao" sort="Cheng, Hao" uniqKey="Cheng H" first="Hao" last="Cheng">Hao Cheng</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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