The Antimalarial Chloroquine Suppresses LPS-Induced NLRP3 Inflammasome Activation and Confers Protection against Murine Endotoxic Shock.
Identifieur interne : 000380 ( Ncbi/Merge ); précédent : 000379; suivant : 000381The Antimalarial Chloroquine Suppresses LPS-Induced NLRP3 Inflammasome Activation and Confers Protection against Murine Endotoxic Shock.
Auteurs : Xiaoli Chen [République populaire de Chine] ; Ning Wang [République populaire de Chine] ; Yuanfeng Zhu [République populaire de Chine] ; Yongling Lu [République populaire de Chine] ; Xin Liu [République populaire de Chine] ; Jiang Zheng [République populaire de Chine]Source :
- Mediators of inflammation [ 1466-1861 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux, Anti-inflammatoires (usage thérapeutique), Antipaludiques (usage thérapeutique), Chloroquine (usage thérapeutique), Inflammasomes (), Inflammasomes (métabolisme), Interleukine-1 bêta (métabolisme), Interleukine-18 (métabolisme), Lipopolysaccharides (pharmacologie), Macrophages (), Macrophages (métabolisme), Mâle, Protéine-3 de la famille des NLR contenant un domaine pyrine (métabolisme), Souris, Souris de lignée BALB C, Test ELISA, Transduction du signal ().
- MESH :
- métabolisme : Inflammasomes, Interleukine-1 bêta, Interleukine-18, Macrophages, Protéine-3 de la famille des NLR contenant un domaine pyrine.
- pharmacologie : Lipopolysaccharides.
- usage thérapeutique : Anti-inflammatoires, Antipaludiques, Chloroquine.
- Animaux, Inflammasomes, Macrophages, Mâle, Souris, Souris de lignée BALB C, Test ELISA, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Anti-Inflammatory Agents (therapeutic use), Antimalarials (therapeutic use), Chloroquine (therapeutic use), Enzyme-Linked Immunosorbent Assay, Inflammasomes (drug effects), Inflammasomes (metabolism), Interleukin-18 (metabolism), Interleukin-1beta (metabolism), Lipopolysaccharides (pharmacology), Macrophages (drug effects), Macrophages (metabolism), Male, Mice, Mice, Inbred BALB C, NLR Family, Pyrin Domain-Containing 3 Protein (metabolism), Signal Transduction (drug effects).
- MESH :
- chemical , drug effects : Inflammasomes.
- chemical , metabolism : Inflammasomes, Interleukin-18, Interleukin-1beta, NLR Family, Pyrin Domain-Containing 3 Protein.
- chemical , pharmacology : Lipopolysaccharides.
- chemical , therapeutic use : Anti-Inflammatory Agents, Antimalarials, Chloroquine.
- drug effects : Macrophages, Signal Transduction.
- metabolism : Macrophages.
- Animals, Enzyme-Linked Immunosorbent Assay, Male, Mice, Mice, Inbred BALB C.
Abstract
Activation of the NLRP3 inflammasome, which catalyzes maturation of proinflammatory cytokines like IL-1β and IL-18, is implicated and essentially involved in many kinds of inflammatory disorders. Chloroquine (CQ) is a traditional antimalarial drug and also possesses an anti-inflammatory property. In this study, we investigated whether CQ suppresses NLRP3 inflammasome activation and thereby confers protection against murine endotoxic shock. CQ attenuated NF-κB and MAPK activation and prohibited expression of IL-1β, IL-18, and Nlrp3 in LPS treated murine bone marrow-derived macrophages (BMDMs), demonstrating its inhibitory effect on the priming signal of NLRP3 activation. Then, CQ was shown to inhibit caspase-1 activation and ASC specks formation in BMDMs, which indicates that CQ also suppresses inflammasome assembly, the second signal for NLRP3 inflammasome activation. In a murine endotoxic shock model, CQ effectively improved survival and markedly reduced IL-1β and IL-18 production in serum, peritoneal fluid, and lung tissues. Moreover, CQ reduced protein levels of NLRP3 and caspases-1 p10 in lung homogenates of mice with endotoxic shock, which may possibly explain its anti-inflammatory activity and life protection efficacy in vivo. Overall, our results demonstrate a new role of CQ that facilitates negative regulation on NLRP3 inflammasome, which thereby confers protection against lethal endotoxic shock.
DOI: 10.1155/2017/6543237
PubMed: 28321151
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000171
- to stream PubMed, to step Curation: 000171
- to stream PubMed, to step Checkpoint: 000142
Links to Exploration step
pubmed:28321151Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The Antimalarial Chloroquine Suppresses LPS-Induced NLRP3 Inflammasome Activation and Confers Protection against Murine Endotoxic Shock.</title><author><name sortKey="Chen, Xiaoli" sort="Chen, Xiaoli" uniqKey="Chen X" first="Xiaoli" last="Chen">Xiaoli Chen</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Ning" sort="Wang, Ning" uniqKey="Wang N" first="Ning" last="Wang">Ning Wang</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Zhu, Yuanfeng" sort="Zhu, Yuanfeng" uniqKey="Zhu Y" first="Yuanfeng" last="Zhu">Yuanfeng Zhu</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Lu, Yongling" sort="Lu, Yongling" uniqKey="Lu Y" first="Yongling" last="Lu">Yongling Lu</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Xin" sort="Liu, Xin" uniqKey="Liu X" first="Xin" last="Liu">Xin Liu</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Zheng, Jiang" sort="Zheng, Jiang" uniqKey="Zheng J" first="Jiang" last="Zheng">Jiang Zheng</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28321151</idno><idno type="pmid">28321151</idno><idno type="doi">10.1155/2017/6543237</idno><idno type="wicri:Area/PubMed/Corpus">000171</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000171</idno><idno type="wicri:Area/PubMed/Curation">000171</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000171</idno><idno type="wicri:Area/PubMed/Checkpoint">000142</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000142</idno><idno type="wicri:Area/Ncbi/Merge">000380</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The Antimalarial Chloroquine Suppresses LPS-Induced NLRP3 Inflammasome Activation and Confers Protection against Murine Endotoxic Shock.</title><author><name sortKey="Chen, Xiaoli" sort="Chen, Xiaoli" uniqKey="Chen X" first="Xiaoli" last="Chen">Xiaoli Chen</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Ning" sort="Wang, Ning" uniqKey="Wang N" first="Ning" last="Wang">Ning Wang</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Zhu, Yuanfeng" sort="Zhu, Yuanfeng" uniqKey="Zhu Y" first="Yuanfeng" last="Zhu">Yuanfeng Zhu</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Lu, Yongling" sort="Lu, Yongling" uniqKey="Lu Y" first="Yongling" last="Lu">Yongling Lu</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Xin" sort="Liu, Xin" uniqKey="Liu X" first="Xin" last="Liu">Xin Liu</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author><author><name sortKey="Zheng, Jiang" sort="Zheng, Jiang" uniqKey="Zheng J" first="Jiang" last="Zheng">Jiang Zheng</name><affiliation wicri:level="1"><nlm:affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038</wicri:regionArea><wicri:noRegion>Chongqing 400038</wicri:noRegion></affiliation></author></analytic><series><title level="j">Mediators of inflammation</title><idno type="eISSN">1466-1861</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Anti-Inflammatory Agents (therapeutic use)</term><term>Antimalarials (therapeutic use)</term><term>Chloroquine (therapeutic use)</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Inflammasomes (drug effects)</term><term>Inflammasomes (metabolism)</term><term>Interleukin-18 (metabolism)</term><term>Interleukin-1beta (metabolism)</term><term>Lipopolysaccharides (pharmacology)</term><term>Macrophages (drug effects)</term><term>Macrophages (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>NLR Family, Pyrin Domain-Containing 3 Protein (metabolism)</term><term>Signal Transduction (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anti-inflammatoires (usage thérapeutique)</term><term>Antipaludiques (usage thérapeutique)</term><term>Chloroquine (usage thérapeutique)</term><term>Inflammasomes ()</term><term>Inflammasomes (métabolisme)</term><term>Interleukine-1 bêta (métabolisme)</term><term>Interleukine-18 (métabolisme)</term><term>Lipopolysaccharides (pharmacologie)</term><term>Macrophages ()</term><term>Macrophages (métabolisme)</term><term>Mâle</term><term>Protéine-3 de la famille des NLR contenant un domaine pyrine (métabolisme)</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Test ELISA</term><term>Transduction du signal ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Inflammasomes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Inflammasomes</term><term>Interleukin-18</term><term>Interleukin-1beta</term><term>NLR Family, Pyrin Domain-Containing 3 Protein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Lipopolysaccharides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>Antimalarials</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Macrophages</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Inflammasomes</term><term>Interleukine-1 bêta</term><term>Interleukine-18</term><term>Macrophages</term><term>Protéine-3 de la famille des NLR contenant un domaine pyrine</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Lipopolysaccharides</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Anti-inflammatoires</term><term>Antipaludiques</term><term>Chloroquine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Inflammasomes</term><term>Macrophages</term><term>Mâle</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Test ELISA</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Activation of the NLRP3 inflammasome, which catalyzes maturation of proinflammatory cytokines like IL-1<i>β</i> and IL-18, is implicated and essentially involved in many kinds of inflammatory disorders. Chloroquine (CQ) is a traditional antimalarial drug and also possesses an anti-inflammatory property. In this study, we investigated whether CQ suppresses NLRP3 inflammasome activation and thereby confers protection against murine endotoxic shock. CQ attenuated NF-<i>κ</i>B and MAPK activation and prohibited expression of IL-1<i>β</i>, IL-18, and <i>Nlrp3</i> in LPS treated murine bone marrow-derived macrophages (BMDMs), demonstrating its inhibitory effect on the priming signal of NLRP3 activation. Then, CQ was shown to inhibit caspase-1 activation and ASC specks formation in BMDMs, which indicates that CQ also suppresses inflammasome assembly, the second signal for NLRP3 inflammasome activation. In a murine endotoxic shock model, CQ effectively improved survival and markedly reduced IL-1<i>β</i> and IL-18 production in serum, peritoneal fluid, and lung tissues. Moreover, CQ reduced protein levels of NLRP3 and caspases-1 p10 in lung homogenates of mice with endotoxic shock, which may possibly explain its anti-inflammatory activity and life protection efficacy in vivo. Overall, our results demonstrate a new role of CQ that facilitates negative regulation on NLRP3 inflammasome, which thereby confers protection against lethal endotoxic shock.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28321151</PMID><DateCompleted><Year>2017</Year><Month>06</Month><Day>05</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1466-1861</ISSN><JournalIssue CitedMedium="Internet"><Volume>2017</Volume><PubDate><Year>2017</Year></PubDate></JournalIssue><Title>Mediators of inflammation</Title><ISOAbbreviation>Mediators Inflamm.</ISOAbbreviation></Journal><ArticleTitle>The Antimalarial Chloroquine Suppresses LPS-Induced NLRP3 Inflammasome Activation and Confers Protection against Murine Endotoxic Shock.</ArticleTitle><Pagination><MedlinePgn>6543237</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1155/2017/6543237</ELocationID><Abstract><AbstractText>Activation of the NLRP3 inflammasome, which catalyzes maturation of proinflammatory cytokines like IL-1<i>β</i> and IL-18, is implicated and essentially involved in many kinds of inflammatory disorders. Chloroquine (CQ) is a traditional antimalarial drug and also possesses an anti-inflammatory property. In this study, we investigated whether CQ suppresses NLRP3 inflammasome activation and thereby confers protection against murine endotoxic shock. CQ attenuated NF-<i>κ</i>B and MAPK activation and prohibited expression of IL-1<i>β</i>, IL-18, and <i>Nlrp3</i> in LPS treated murine bone marrow-derived macrophages (BMDMs), demonstrating its inhibitory effect on the priming signal of NLRP3 activation. Then, CQ was shown to inhibit caspase-1 activation and ASC specks formation in BMDMs, which indicates that CQ also suppresses inflammasome assembly, the second signal for NLRP3 inflammasome activation. In a murine endotoxic shock model, CQ effectively improved survival and markedly reduced IL-1<i>β</i> and IL-18 production in serum, peritoneal fluid, and lung tissues. Moreover, CQ reduced protein levels of NLRP3 and caspases-1 p10 in lung homogenates of mice with endotoxic shock, which may possibly explain its anti-inflammatory activity and life protection efficacy in vivo. Overall, our results demonstrate a new role of CQ that facilitates negative regulation on NLRP3 inflammasome, which thereby confers protection against lethal endotoxic shock.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Xiaoli</ForeName><Initials>X</Initials><Identifier Source="ORCID">0000-0003-3513-3551</Identifier><AffiliationInfo><Affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Ning</ForeName><Initials>N</Initials><Identifier Source="ORCID">0000-0002-9913-5006</Identifier><AffiliationInfo><Affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Yuanfeng</ForeName><Initials>Y</Initials><Identifier Source="ORCID">0000-0002-6414-6709</Identifier><AffiliationInfo><Affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Yongling</ForeName><Initials>Y</Initials><Identifier Source="ORCID">0000-0003-0092-7036</Identifier><AffiliationInfo><Affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xin</ForeName><Initials>X</Initials><Identifier Source="ORCID">0000-0002-2986-6364</Identifier><AffiliationInfo><Affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zheng</LastName><ForeName>Jiang</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0002-9049-2234</Identifier><AffiliationInfo><Affiliation>Medical Research Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mediators Inflamm</MedlineTA><NlmUniqueID>9209001</NlmUniqueID><ISSNLinking>0962-9351</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000893">Anti-Inflammatory Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000962">Antimalarials</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058847">Inflammasomes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020382">Interleukin-18</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053583">Interleukin-1beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071199">NLR Family, Pyrin Domain-Containing 3 Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000962" MajorTopicYN="N">Antimalarials</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004797" MajorTopicYN="N">Enzyme-Linked Immunosorbent Assay</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058847" MajorTopicYN="N">Inflammasomes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020382" MajorTopicYN="N">Interleukin-18</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053583" MajorTopicYN="N">Interleukin-1beta</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000071199" MajorTopicYN="N">NLR Family, Pyrin Domain-Containing 3 Protein</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors declare that there are no competing interests regarding the publication of this paper.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>09</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>01</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>01</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>3</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>3</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>6</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28321151</ArticleId><ArticleId IdType="doi">10.1155/2017/6543237</ArticleId><ArticleId IdType="pmc">PMC5340938</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Cytokine. 2015 Oct;75(2):280-90</Citation><ArticleIdList><ArticleId IdType="pubmed">26194067</ArticleId></ArticleIdList></Reference><Reference><Citation>Int J Mol Sci. 2015 Apr 10;16(4):8102-9</Citation><ArticleIdList><ArticleId IdType="pubmed">25867480</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Commun. 2014 Aug 20;5:4738</Citation><ArticleIdList><ArticleId IdType="pubmed">25141024</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Immunol. 2011 Jul 19;12(8):695-708</Citation><ArticleIdList><ArticleId IdType="pubmed">21772278</ArticleId></ArticleIdList></Reference><Reference><Citation>Cytokine. 2015 Nov;76(1):25-37</Citation><ArticleIdList><ArticleId IdType="pubmed">26185894</ArticleId></ArticleIdList></Reference><Reference><Citation>Crit Care. 2013 Jul 24;17(4):R160</Citation><ArticleIdList><ArticleId IdType="pubmed">23883625</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunity. 2013 Jun 27;38(6):1142-53</Citation><ArticleIdList><ArticleId IdType="pubmed">23809161</ArticleId></ArticleIdList></Reference><Reference><Citation>FEBS Lett. 2012 Apr 5;586(7):1022-6</Citation><ArticleIdList><ArticleId IdType="pubmed">22569257</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Immunol. 2011 Jun 19;12(8):709-14</Citation><ArticleIdList><ArticleId IdType="pubmed">21772279</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Death Differ. 2006 Feb;13(2):236-49</Citation><ArticleIdList><ArticleId IdType="pubmed">16037825</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2000 Jun;68(6):3502-8</Citation><ArticleIdList><ArticleId IdType="pubmed">10816504</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochem Biophys Res Commun. 2015 Mar 13;458(3):700-6</Citation><ArticleIdList><ArticleId IdType="pubmed">25686493</ArticleId></ArticleIdList></Reference><Reference><Citation>Bull Cancer. 2015 Sep;102(9):780-5</Citation><ArticleIdList><ArticleId IdType="pubmed">26235415</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Cell Mol Biol. 2014 Apr;50(4):723-36</Citation><ArticleIdList><ArticleId IdType="pubmed">24168260</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunity. 2014 Apr 17;40(4):463-75</Citation><ArticleIdList><ArticleId IdType="pubmed">24745331</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Cell Dev Biol. 2012;28:137-61</Citation><ArticleIdList><ArticleId IdType="pubmed">22974247</ArticleId></ArticleIdList></Reference><Reference><Citation>Int Immunopharmacol. 2004 Feb;4(2):223-34</Citation><ArticleIdList><ArticleId IdType="pubmed">14996414</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Immunol. 2012;274(1-2):121-9</Citation><ArticleIdList><ArticleId IdType="pubmed">22341560</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Immunol. 2010 Feb;10(2):89-102</Citation><ArticleIdList><ArticleId IdType="pubmed">20081871</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunol Lett. 2013 Jun;153(1-2):50-7</Citation><ArticleIdList><ArticleId IdType="pubmed">23891850</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Crit Care Med. 2014 Feb 1;189(3):282-91</Citation><ArticleIdList><ArticleId IdType="pubmed">24456467</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Mol Immunol. 2016 Mar;13(2):148-59</Citation><ArticleIdList><ArticleId IdType="pubmed">26549800</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol Methods. 2015 Aug;423:3-11</Citation><ArticleIdList><ArticleId IdType="pubmed">25862606</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Signal. 2001 Feb;13(2):85-94</Citation><ArticleIdList><ArticleId IdType="pubmed">11257452</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2009 Jul 15;183(2):787-91</Citation><ArticleIdList><ArticleId IdType="pubmed">19570822</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2006 Mar 9;440(7081):228-32</Citation><ArticleIdList><ArticleId IdType="pubmed">16407890</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Med. 2014 Dec 16;20 Suppl 1:S43-58</Citation><ArticleIdList><ArticleId IdType="pubmed">25549233</ArticleId></ArticleIdList></Reference><Reference><Citation>Int Immunopharmacol. 2014 Aug;21(2):328-35</Citation><ArticleIdList><ArticleId IdType="pubmed">24859061</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunity. 2006 Mar;24(3):317-27</Citation><ArticleIdList><ArticleId IdType="pubmed">16546100</ArticleId></ArticleIdList></Reference><Reference><Citation>FASEB J. 2015 Sep;29(9):3863-75</Citation><ArticleIdList><ArticleId IdType="pubmed">26045547</ArticleId></ArticleIdList></Reference><Reference><Citation>J Ethnopharmacol. 2013 Jan 30;145(2):626-37</Citation><ArticleIdList><ArticleId IdType="pubmed">23237934</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2004 Jun 8;101(23):8815-20</Citation><ArticleIdList><ArticleId IdType="pubmed">15161979</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2014 Mar 13;156(6):1193-206</Citation><ArticleIdList><ArticleId IdType="pubmed">24630722</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Med. 2015 Jul;21(7):677-87</Citation><ArticleIdList><ArticleId IdType="pubmed">26121197</ArticleId></ArticleIdList></Reference><Reference><Citation>Inflammation. 2015 Apr;38(2):745-55</Citation><ArticleIdList><ArticleId IdType="pubmed">25085745</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Physiol Cell Physiol. 2013 Jul 15;305(2):C182-9</Citation><ArticleIdList><ArticleId IdType="pubmed">23636457</ArticleId></ArticleIdList></Reference><Reference><Citation>Shock. 2012 Jan;37(1):124-5</Citation><ArticleIdList><ArticleId IdType="pubmed">22157943</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2012 Oct 5;287(41):34474-83</Citation><ArticleIdList><ArticleId IdType="pubmed">22898816</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochem Pharmacol. 2013 Aug 1;86(3):410-8</Citation><ArticleIdList><ArticleId IdType="pubmed">23707973</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Chen, Xiaoli" sort="Chen, Xiaoli" uniqKey="Chen X" first="Xiaoli" last="Chen">Xiaoli Chen</name></noRegion><name sortKey="Liu, Xin" sort="Liu, Xin" uniqKey="Liu X" first="Xin" last="Liu">Xin Liu</name><name sortKey="Lu, Yongling" sort="Lu, Yongling" uniqKey="Lu Y" first="Yongling" last="Lu">Yongling Lu</name><name sortKey="Wang, Ning" sort="Wang, Ning" uniqKey="Wang N" first="Ning" last="Wang">Ning Wang</name><name sortKey="Zheng, Jiang" sort="Zheng, Jiang" uniqKey="Zheng J" first="Jiang" last="Zheng">Jiang Zheng</name><name sortKey="Zhu, Yuanfeng" sort="Zhu, Yuanfeng" uniqKey="Zhu Y" first="Yuanfeng" last="Zhu">Yuanfeng Zhu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Ncbi/Merge
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000380 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd -nk 000380 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= Ncbi
|étape= Merge
|type= RBID
|clé= pubmed:28321151
|texte= The Antimalarial Chloroquine Suppresses LPS-Induced NLRP3 Inflammasome Activation and Confers Protection against Murine Endotoxic Shock.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/RBID.i -Sk "pubmed:28321151" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |