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 : 000311 ( Main/Merge ); précédent : 000310; suivant : 000312Transient 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.
Url:
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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