The nucleotide-binding domain, leucine-rich repeat protein 3 inflammasome/IL-1 receptor I axis mediates innate, but not adaptive, immune responses after exposure to particulate matter under 10 μm.
Identifieur interne : 000588 ( PubMed/Corpus ); précédent : 000587; suivant : 000589The nucleotide-binding domain, leucine-rich repeat protein 3 inflammasome/IL-1 receptor I axis mediates innate, but not adaptive, immune responses after exposure to particulate matter under 10 μm.
Auteurs : Jeremy A. Hirota ; Matthew J. Gold ; Paul R. Hiebert ; Leigh G. Parkinson ; Tracee Wee ; Dirk Smith ; Phil M. Hansbro ; Chris Carlsten ; Stephan Vaneeden ; Don D. Sin ; Kelly M. Mcnagny ; Darryl A. KnightSource :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2015.
English descriptors
- KwdEn :
- Adaptive Immunity (drug effects), Animals, Asthma (chemically induced), Asthma (immunology), Asthma (pathology), Carrier Proteins (immunology), Cell Line, Transformed, Cytokines (immunology), Dendritic Cells (immunology), Dendritic Cells (pathology), Humans, Immunity, Innate (drug effects), Inflammasomes (immunology), Mice, Mice, Inbred BALB C, NLR Family, Pyrin Domain-Containing 3 Protein, Particulate Matter (adverse effects), Particulate Matter (pharmacology), Receptors, Interleukin-1 Type I (immunology), Respiratory Mucosa (immunology), Respiratory Mucosa (pathology), Signal Transduction (immunology).
- MESH :
- chemical , adverse effects : Particulate Matter.
- chemical , immunology : Carrier Proteins, Cytokines, Inflammasomes, Receptors, Interleukin-1 Type I.
- chemically induced : Asthma.
- drug effects : Adaptive Immunity, Immunity, Innate.
- immunology : Asthma, Dendritic Cells, Respiratory Mucosa, Signal Transduction.
- pathology : Asthma, Dendritic Cells, Respiratory Mucosa.
- chemical , pharmacology : Particulate Matter.
- Animals, Cell Line, Transformed, Humans, Mice, Mice, Inbred BALB C, NLR Family, Pyrin Domain-Containing 3 Protein.
Abstract
Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. Inhaled PM induces innate immune responses by airway epithelial cells that may lead to the exacerbation or de novo development of airway disease. We have previously shown that 10-μm PM (PM10) activates the nucleotide-binding domain, leucine-rich repeat protein (NLRP) 3 inflammasome in human airway epithelial cells. Our objective was to determine the innate and adaptive immune responses mediated by the airway epithelium NLRP3 inflammasome in response to PM10 exposure. Using in vitro cultures of human airway epithelial cells and in vivo studies with wild-type and Nlrp3(-/-) mice, we investigated the downstream consequences of PM10-induced NLPR3 inflammasome activation on cytokine production, cellular inflammation, dendritic cell activation, and PM10-facilitated allergic sensitization. PM10 activates an NLRP3 inflammasome/IL-1 receptor I (IL-1RI) axis in airway epithelial cells, resulting in IL-1β, CC chemokine ligand-20, and granulocyte/macrophage colony-stimulating factor production, which is associated with dendritic cell activation and lung neutrophilia. Despite these profound innate immune responses in the airway epithelium, the NLRP3 inflammasome/IL-1RI axis is dispensable for PM10-facilitated allergic sensitization. We demonstrate the importance of the lung NLRP3 inflammasome in mediating PM10 exposure-associated innate, but not adaptive, immune responses. Our study highlights a mechanism by which PM10 exposure can contribute to the exacerbation of airway disease, but not PM10-facilitated allergic sensitization.
DOI: 10.1165/rcmb.2014-0158OC
PubMed: 24988285
Links to Exploration step
pubmed:24988285Le document en format XML
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Parkinson</name></author><author><name sortKey="Wee, Tracee" sort="Wee, Tracee" uniqKey="Wee T" first="Tracee" last="Wee">Tracee Wee</name></author><author><name sortKey="Smith, Dirk" sort="Smith, Dirk" uniqKey="Smith D" first="Dirk" last="Smith">Dirk Smith</name></author><author><name sortKey="Hansbro, Phil M" sort="Hansbro, Phil M" uniqKey="Hansbro P" first="Phil M" last="Hansbro">Phil M. Hansbro</name></author><author><name sortKey="Carlsten, Chris" sort="Carlsten, Chris" uniqKey="Carlsten C" first="Chris" last="Carlsten">Chris Carlsten</name></author><author><name sortKey="Vaneeden, Stephan" sort="Vaneeden, Stephan" uniqKey="Vaneeden S" first="Stephan" last="Vaneeden">Stephan Vaneeden</name></author><author><name sortKey="Sin, Don D" sort="Sin, Don D" uniqKey="Sin D" first="Don D" last="Sin">Don D. Sin</name></author><author><name sortKey="Mcnagny, Kelly M" sort="Mcnagny, Kelly M" uniqKey="Mcnagny K" first="Kelly M" last="Mcnagny">Kelly M. 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Hirota</name><affiliation><nlm:affiliation>1 James Hogg Research Centre.</nlm:affiliation></affiliation></author><author><name sortKey="Gold, Matthew J" sort="Gold, Matthew J" uniqKey="Gold M" first="Matthew J" last="Gold">Matthew J. Gold</name></author><author><name sortKey="Hiebert, Paul R" sort="Hiebert, Paul R" uniqKey="Hiebert P" first="Paul R" last="Hiebert">Paul R. Hiebert</name></author><author><name sortKey="Parkinson, Leigh G" sort="Parkinson, Leigh G" uniqKey="Parkinson L" first="Leigh G" last="Parkinson">Leigh G. Parkinson</name></author><author><name sortKey="Wee, Tracee" sort="Wee, Tracee" uniqKey="Wee T" first="Tracee" last="Wee">Tracee Wee</name></author><author><name sortKey="Smith, Dirk" sort="Smith, Dirk" uniqKey="Smith D" first="Dirk" last="Smith">Dirk Smith</name></author><author><name sortKey="Hansbro, Phil M" sort="Hansbro, Phil M" uniqKey="Hansbro P" first="Phil M" last="Hansbro">Phil M. Hansbro</name></author><author><name sortKey="Carlsten, Chris" sort="Carlsten, Chris" uniqKey="Carlsten C" first="Chris" last="Carlsten">Chris Carlsten</name></author><author><name sortKey="Vaneeden, Stephan" sort="Vaneeden, Stephan" uniqKey="Vaneeden S" first="Stephan" last="Vaneeden">Stephan Vaneeden</name></author><author><name sortKey="Sin, Don D" sort="Sin, Don D" uniqKey="Sin D" first="Don D" last="Sin">Don D. Sin</name></author><author><name sortKey="Mcnagny, Kelly M" sort="Mcnagny, Kelly M" uniqKey="Mcnagny K" first="Kelly M" last="Mcnagny">Kelly M. Mcnagny</name></author><author><name sortKey="Knight, Darryl A" sort="Knight, Darryl A" uniqKey="Knight D" first="Darryl A" last="Knight">Darryl A. Knight</name></author></analytic><series><title level="j">American journal of respiratory cell and molecular biology</title><idno type="eISSN">1535-4989</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptive Immunity (drug effects)</term><term>Animals</term><term>Asthma (chemically induced)</term><term>Asthma (immunology)</term><term>Asthma (pathology)</term><term>Carrier Proteins (immunology)</term><term>Cell Line, Transformed</term><term>Cytokines (immunology)</term><term>Dendritic Cells (immunology)</term><term>Dendritic Cells (pathology)</term><term>Humans</term><term>Immunity, Innate (drug effects)</term><term>Inflammasomes (immunology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>NLR Family, Pyrin Domain-Containing 3 Protein</term><term>Particulate Matter (adverse effects)</term><term>Particulate Matter (pharmacology)</term><term>Receptors, Interleukin-1 Type I (immunology)</term><term>Respiratory Mucosa (immunology)</term><term>Respiratory Mucosa (pathology)</term><term>Signal Transduction (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Particulate Matter</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Carrier Proteins</term><term>Cytokines</term><term>Inflammasomes</term><term>Receptors, Interleukin-1 Type I</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Asthma</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Adaptive Immunity</term><term>Immunity, Innate</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Asthma</term><term>Dendritic Cells</term><term>Respiratory Mucosa</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Asthma</term><term>Dendritic Cells</term><term>Respiratory Mucosa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Particulate Matter</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Transformed</term><term>Humans</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>NLR Family, Pyrin Domain-Containing 3 Protein</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. Inhaled PM induces innate immune responses by airway epithelial cells that may lead to the exacerbation or de novo development of airway disease. We have previously shown that 10-μm PM (PM10) activates the nucleotide-binding domain, leucine-rich repeat protein (NLRP) 3 inflammasome in human airway epithelial cells. Our objective was to determine the innate and adaptive immune responses mediated by the airway epithelium NLRP3 inflammasome in response to PM10 exposure. Using in vitro cultures of human airway epithelial cells and in vivo studies with wild-type and Nlrp3(-/-) mice, we investigated the downstream consequences of PM10-induced NLPR3 inflammasome activation on cytokine production, cellular inflammation, dendritic cell activation, and PM10-facilitated allergic sensitization. PM10 activates an NLRP3 inflammasome/IL-1 receptor I (IL-1RI) axis in airway epithelial cells, resulting in IL-1β, CC chemokine ligand-20, and granulocyte/macrophage colony-stimulating factor production, which is associated with dendritic cell activation and lung neutrophilia. Despite these profound innate immune responses in the airway epithelium, the NLRP3 inflammasome/IL-1RI axis is dispensable for PM10-facilitated allergic sensitization. We demonstrate the importance of the lung NLRP3 inflammasome in mediating PM10 exposure-associated innate, but not adaptive, immune responses. Our study highlights a mechanism by which PM10 exposure can contribute to the exacerbation of airway disease, but not PM10-facilitated allergic sensitization.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24988285</PMID><DateCreated><Year>2015</Year><Month>01</Month><Day>01</Day></DateCreated><DateCompleted><Year>2015</Year><Month>03</Month><Day>11</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1535-4989</ISSN><JournalIssue CitedMedium="Internet"><Volume>52</Volume><Issue>1</Issue><PubDate><Year>2015</Year><Month>Jan</Month></PubDate></JournalIssue><Title>American journal of respiratory cell and molecular biology</Title><ISOAbbreviation>Am. J. Respir. Cell Mol. Biol.</ISOAbbreviation></Journal><ArticleTitle>The nucleotide-binding domain, leucine-rich repeat protein 3 inflammasome/IL-1 receptor I axis mediates innate, but not adaptive, immune responses after exposure to particulate matter under 10 μm.</ArticleTitle><Pagination><MedlinePgn>96-105</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1165/rcmb.2014-0158OC</ELocationID><Abstract><AbstractText>Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. Inhaled PM induces innate immune responses by airway epithelial cells that may lead to the exacerbation or de novo development of airway disease. We have previously shown that 10-μm PM (PM10) activates the nucleotide-binding domain, leucine-rich repeat protein (NLRP) 3 inflammasome in human airway epithelial cells. Our objective was to determine the innate and adaptive immune responses mediated by the airway epithelium NLRP3 inflammasome in response to PM10 exposure. Using in vitro cultures of human airway epithelial cells and in vivo studies with wild-type and Nlrp3(-/-) mice, we investigated the downstream consequences of PM10-induced NLPR3 inflammasome activation on cytokine production, cellular inflammation, dendritic cell activation, and PM10-facilitated allergic sensitization. PM10 activates an NLRP3 inflammasome/IL-1 receptor I (IL-1RI) axis in airway epithelial cells, resulting in IL-1β, CC chemokine ligand-20, and granulocyte/macrophage colony-stimulating factor production, which is associated with dendritic cell activation and lung neutrophilia. Despite these profound innate immune responses in the airway epithelium, the NLRP3 inflammasome/IL-1RI axis is dispensable for PM10-facilitated allergic sensitization. We demonstrate the importance of the lung NLRP3 inflammasome in mediating PM10 exposure-associated innate, but not adaptive, immune responses. Our study highlights a mechanism by which PM10 exposure can contribute to the exacerbation of airway disease, but not PM10-facilitated allergic sensitization.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hirota</LastName><ForeName>Jeremy A</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>1 James Hogg Research Centre.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gold</LastName><ForeName>Matthew J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Hiebert</LastName><ForeName>Paul R</ForeName><Initials>PR</Initials></Author><Author ValidYN="Y"><LastName>Parkinson</LastName><ForeName>Leigh G</ForeName><Initials>LG</Initials></Author><Author ValidYN="Y"><LastName>Wee</LastName><ForeName>Tracee</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Smith</LastName><ForeName>Dirk</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Hansbro</LastName><ForeName>Phil M</ForeName><Initials>PM</Initials></Author><Author ValidYN="Y"><LastName>Carlsten</LastName><ForeName>Chris</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>VanEeden</LastName><ForeName>Stephan</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Sin</LastName><ForeName>Don D</ForeName><Initials>DD</Initials></Author><Author ValidYN="Y"><LastName>McNagny</LastName><ForeName>Kelly M</ForeName><Initials>KM</Initials></Author><Author ValidYN="Y"><LastName>Knight</LastName><ForeName>Darryl A</ForeName><Initials>DA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Respir Cell Mol Biol</MedlineTA><NlmUniqueID>8917225</NlmUniqueID><ISSNLinking>1044-1549</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C508590">IL1R1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C583355">IL1R1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058847">Inflammasomes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071199">NLR Family, Pyrin Domain-Containing 3 Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C453881">NLRP3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C492716">Nlrp3 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D052638">Particulate Matter</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053573">Receptors, Interleukin-1 Type I</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D056704" MajorTopicYN="N">Adaptive Immunity</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001249" MajorTopicYN="N">Asthma</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002461" MajorTopicYN="N">Cell Line, Transformed</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003713" MajorTopicYN="N">Dendritic Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058847" MajorTopicYN="N">Inflammasomes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></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></MeshHeading><MeshHeading><DescriptorName UI="D052638" MajorTopicYN="N">Particulate Matter</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053573" MajorTopicYN="N">Receptors, Interleukin-1 Type I</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020545" MajorTopicYN="N">Respiratory Mucosa</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">air pollution</Keyword><Keyword MajorTopicYN="N">airway epithelium</Keyword><Keyword MajorTopicYN="N">allergic sensitization</Keyword><Keyword MajorTopicYN="N">asthma</Keyword><Keyword MajorTopicYN="N">human</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>7</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>7</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>3</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24988285</ArticleId><ArticleId IdType="doi">10.1165/rcmb.2014-0158OC</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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