Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines.
Identifieur interne : 000366 ( PubMed/Corpus ); précédent : 000365; suivant : 000367Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines.
Auteurs : Christine Schauer ; Christina Janko ; Luis E. Munoz ; Yi Zhao ; Deborah Kienhöfer ; Benjamin Frey ; Michael Lell ; Bernhard Manger ; Jürgen Rech ; Elisabeth Naschberger ; Rikard Holmdahl ; Veit Krenn ; Thomas Harrer ; Ivica Jeremic ; Rostyslav Bilyy ; Georg Schett ; Markus Hoffmann ; Martin HerrmannSource :
- Nature medicine [ 1546-170X ] ; 2014.
English descriptors
- KwdEn :
- Animals, Cell Aggregation (drug effects), Chemokines (metabolism), Cytokines (metabolism), Gout (metabolism), Gout (pathology), Humans, Inflammation (genetics), Inflammation (metabolism), Inflammation (pathology), Mice, Neutrophils (metabolism), Neutrophils (pathology), Respiratory Burst (drug effects), Synovial Fluid (drug effects), Uric Acid (toxicity).
- MESH :
- chemical , metabolism : Chemokines, Cytokines.
- drug effects : Cell Aggregation, Respiratory Burst, Synovial Fluid.
- genetics : Inflammation.
- metabolism : Gout, Inflammation, Neutrophils.
- pathology : Gout, Inflammation, Neutrophils.
- chemical , toxicity : Uric Acid.
- Animals, Humans, Mice.
Abstract
Gout is characterized by an acute inflammatory reaction and the accumulation of neutrophils in response to monosodium urate (MSU) crystals. Inflammation resolves spontaneously within a few days, although MSU crystals can still be detected in the synovial fluid and affected tissues. Here we report that neutrophils recruited to sites of inflammation undergo oxidative burst and form neutrophil extracellular traps (NETs). Under high neutrophil densities, these NETs aggregate and degrade cytokines and chemokines via serine proteases. Tophi, the pathognomonic structures of chronic gout, share characteristics with aggregated NETs, and MSU crystals can induce NETosis and aggregation of NETs. In individuals with impaired NETosis, MSU crystals induce uncontrolled production of inflammatory mediators from neutrophils and persistent inflammation. Furthermore, in models of neutrophilic inflammation, NETosis-deficient mice develop exacerbated and chronic disease that can be reduced by adoptive transfer of aggregated NETs. These findings suggest that aggregated NETs promote the resolution of neutrophilic inflammation by degrading cytokines and chemokines and disrupting neutrophil recruitment and activation.
DOI: 10.1038/nm.3547
PubMed: 24784231
Links to Exploration step
pubmed:24784231Le document en format XML
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[2] Department of Otorhinolaryngology, Head and Neck Surgery, Section for Experimental Oncology and Nanomedicine (SEON), University Hospital Erlangen, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Munoz, Luis E" sort="Munoz, Luis E" uniqKey="Munoz L" first="Luis E" last="Munoz">Luis E. Munoz</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Zhao, Yi" sort="Zhao, Yi" uniqKey="Zhao Y" first="Yi" last="Zhao">Yi Zhao</name><affiliation><nlm:affiliation>1] Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany. [2] Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation></affiliation></author><author><name sortKey="Kienhofer, Deborah" sort="Kienhofer, Deborah" uniqKey="Kienhofer D" first="Deborah" last="Kienhöfer">Deborah Kienhöfer</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Frey, Benjamin" sort="Frey, Benjamin" uniqKey="Frey B" first="Benjamin" last="Frey">Benjamin Frey</name><affiliation><nlm:affiliation>Department of Radiation Oncology, University Hospital Erlangen, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Lell, Michael" sort="Lell, Michael" uniqKey="Lell M" first="Michael" last="Lell">Michael Lell</name><affiliation><nlm:affiliation>Department of Radiology, Friedrich-Alexander University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Manger, Bernhard" sort="Manger, Bernhard" uniqKey="Manger B" first="Bernhard" last="Manger">Bernhard Manger</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Rech, Jurgen" sort="Rech, Jurgen" uniqKey="Rech J" first="Jürgen" last="Rech">Jürgen Rech</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Naschberger, Elisabeth" sort="Naschberger, Elisabeth" uniqKey="Naschberger E" first="Elisabeth" last="Naschberger">Elisabeth Naschberger</name><affiliation><nlm:affiliation>Division of Molecular and Experimental Surgery, Department of Surgery, University of Erlangen Medical Center, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Holmdahl, Rikard" sort="Holmdahl, Rikard" uniqKey="Holmdahl R" first="Rikard" last="Holmdahl">Rikard Holmdahl</name><affiliation><nlm:affiliation>Division of Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.</nlm:affiliation></affiliation></author><author><name sortKey="Krenn, Veit" sort="Krenn, Veit" uniqKey="Krenn V" first="Veit" last="Krenn">Veit Krenn</name><affiliation><nlm:affiliation>Department of Pathology, MVZ of Pathology, Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Harrer, Thomas" sort="Harrer, Thomas" uniqKey="Harrer T" first="Thomas" last="Harrer">Thomas Harrer</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Jeremic, Ivica" sort="Jeremic, Ivica" uniqKey="Jeremic I" first="Ivica" last="Jeremic">Ivica Jeremic</name><affiliation><nlm:affiliation>1] Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany. [2] Institute of Rheumatology, School of Medicine, University of Belgrade, Belgrade, Serbia.</nlm:affiliation></affiliation></author><author><name sortKey="Bilyy, Rostyslav" sort="Bilyy, Rostyslav" uniqKey="Bilyy R" first="Rostyslav" last="Bilyy">Rostyslav Bilyy</name><affiliation><nlm:affiliation>Institute of Cell Biology, National Academy of Sciences of Ukraine, Lviv, Ukraine.</nlm:affiliation></affiliation></author><author><name sortKey="Schett, Georg" sort="Schett, Georg" uniqKey="Schett G" first="Georg" last="Schett">Georg Schett</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Hoffmann, Markus" sort="Hoffmann, Markus" uniqKey="Hoffmann M" first="Markus" last="Hoffmann">Markus Hoffmann</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Herrmann, Martin" sort="Herrmann, Martin" uniqKey="Herrmann M" first="Martin" last="Herrmann">Martin Herrmann</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24784231</idno><idno type="pmid">24784231</idno><idno type="doi">10.1038/nm.3547</idno><idno type="wicri:Area/PubMed/Corpus">000366</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000366</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines.</title><author><name sortKey="Schauer, Christine" sort="Schauer, Christine" uniqKey="Schauer C" first="Christine" last="Schauer">Christine Schauer</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Janko, Christina" sort="Janko, Christina" uniqKey="Janko C" first="Christina" last="Janko">Christina Janko</name><affiliation><nlm:affiliation>1] Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany. [2] Department of Otorhinolaryngology, Head and Neck Surgery, Section for Experimental Oncology and Nanomedicine (SEON), University Hospital Erlangen, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Munoz, Luis E" sort="Munoz, Luis E" uniqKey="Munoz L" first="Luis E" last="Munoz">Luis E. Munoz</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Zhao, Yi" sort="Zhao, Yi" uniqKey="Zhao Y" first="Yi" last="Zhao">Yi Zhao</name><affiliation><nlm:affiliation>1] Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany. [2] Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation></affiliation></author><author><name sortKey="Kienhofer, Deborah" sort="Kienhofer, Deborah" uniqKey="Kienhofer D" first="Deborah" last="Kienhöfer">Deborah Kienhöfer</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Frey, Benjamin" sort="Frey, Benjamin" uniqKey="Frey B" first="Benjamin" last="Frey">Benjamin Frey</name><affiliation><nlm:affiliation>Department of Radiation Oncology, University Hospital Erlangen, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Lell, Michael" sort="Lell, Michael" uniqKey="Lell M" first="Michael" last="Lell">Michael Lell</name><affiliation><nlm:affiliation>Department of Radiology, Friedrich-Alexander University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Manger, Bernhard" sort="Manger, Bernhard" uniqKey="Manger B" first="Bernhard" last="Manger">Bernhard Manger</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Rech, Jurgen" sort="Rech, Jurgen" uniqKey="Rech J" first="Jürgen" last="Rech">Jürgen Rech</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Naschberger, Elisabeth" sort="Naschberger, Elisabeth" uniqKey="Naschberger E" first="Elisabeth" last="Naschberger">Elisabeth Naschberger</name><affiliation><nlm:affiliation>Division of Molecular and Experimental Surgery, Department of Surgery, University of Erlangen Medical Center, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Holmdahl, Rikard" sort="Holmdahl, Rikard" uniqKey="Holmdahl R" first="Rikard" last="Holmdahl">Rikard Holmdahl</name><affiliation><nlm:affiliation>Division of Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.</nlm:affiliation></affiliation></author><author><name sortKey="Krenn, Veit" sort="Krenn, Veit" uniqKey="Krenn V" first="Veit" last="Krenn">Veit Krenn</name><affiliation><nlm:affiliation>Department of Pathology, MVZ of Pathology, Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Harrer, Thomas" sort="Harrer, Thomas" uniqKey="Harrer T" first="Thomas" last="Harrer">Thomas Harrer</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Jeremic, Ivica" sort="Jeremic, Ivica" uniqKey="Jeremic I" first="Ivica" last="Jeremic">Ivica Jeremic</name><affiliation><nlm:affiliation>1] Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany. [2] Institute of Rheumatology, School of Medicine, University of Belgrade, Belgrade, Serbia.</nlm:affiliation></affiliation></author><author><name sortKey="Bilyy, Rostyslav" sort="Bilyy, Rostyslav" uniqKey="Bilyy R" first="Rostyslav" last="Bilyy">Rostyslav Bilyy</name><affiliation><nlm:affiliation>Institute of Cell Biology, National Academy of Sciences of Ukraine, Lviv, Ukraine.</nlm:affiliation></affiliation></author><author><name sortKey="Schett, Georg" sort="Schett, Georg" uniqKey="Schett G" first="Georg" last="Schett">Georg Schett</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Hoffmann, Markus" sort="Hoffmann, Markus" uniqKey="Hoffmann M" first="Markus" last="Hoffmann">Markus Hoffmann</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Herrmann, Martin" sort="Herrmann, Martin" uniqKey="Herrmann M" first="Martin" last="Herrmann">Martin Herrmann</name><affiliation><nlm:affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Nature medicine</title><idno type="eISSN">1546-170X</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Aggregation (drug effects)</term><term>Chemokines (metabolism)</term><term>Cytokines (metabolism)</term><term>Gout (metabolism)</term><term>Gout (pathology)</term><term>Humans</term><term>Inflammation (genetics)</term><term>Inflammation (metabolism)</term><term>Inflammation (pathology)</term><term>Mice</term><term>Neutrophils (metabolism)</term><term>Neutrophils (pathology)</term><term>Respiratory Burst (drug effects)</term><term>Synovial Fluid (drug effects)</term><term>Uric Acid (toxicity)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Chemokines</term><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Aggregation</term><term>Respiratory Burst</term><term>Synovial Fluid</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Gout</term><term>Inflammation</term><term>Neutrophils</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Gout</term><term>Inflammation</term><term>Neutrophils</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Uric Acid</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Mice</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Gout is characterized by an acute inflammatory reaction and the accumulation of neutrophils in response to monosodium urate (MSU) crystals. Inflammation resolves spontaneously within a few days, although MSU crystals can still be detected in the synovial fluid and affected tissues. Here we report that neutrophils recruited to sites of inflammation undergo oxidative burst and form neutrophil extracellular traps (NETs). Under high neutrophil densities, these NETs aggregate and degrade cytokines and chemokines via serine proteases. Tophi, the pathognomonic structures of chronic gout, share characteristics with aggregated NETs, and MSU crystals can induce NETosis and aggregation of NETs. In individuals with impaired NETosis, MSU crystals induce uncontrolled production of inflammatory mediators from neutrophils and persistent inflammation. Furthermore, in models of neutrophilic inflammation, NETosis-deficient mice develop exacerbated and chronic disease that can be reduced by adoptive transfer of aggregated NETs. These findings suggest that aggregated NETs promote the resolution of neutrophilic inflammation by degrading cytokines and chemokines and disrupting neutrophil recruitment and activation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24784231</PMID><DateCreated><Year>2014</Year><Month>05</Month><Day>08</Day></DateCreated><DateCompleted><Year>2014</Year><Month>06</Month><Day>23</Day></DateCompleted><DateRevised><Year>2014</Year><Month>07</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1546-170X</ISSN><JournalIssue CitedMedium="Internet"><Volume>20</Volume><Issue>5</Issue><PubDate><Year>2014</Year><Month>May</Month></PubDate></JournalIssue><Title>Nature medicine</Title><ISOAbbreviation>Nat. Med.</ISOAbbreviation></Journal><ArticleTitle>Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines.</ArticleTitle><Pagination><MedlinePgn>511-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/nm.3547</ELocationID><Abstract><AbstractText>Gout is characterized by an acute inflammatory reaction and the accumulation of neutrophils in response to monosodium urate (MSU) crystals. Inflammation resolves spontaneously within a few days, although MSU crystals can still be detected in the synovial fluid and affected tissues. Here we report that neutrophils recruited to sites of inflammation undergo oxidative burst and form neutrophil extracellular traps (NETs). Under high neutrophil densities, these NETs aggregate and degrade cytokines and chemokines via serine proteases. Tophi, the pathognomonic structures of chronic gout, share characteristics with aggregated NETs, and MSU crystals can induce NETosis and aggregation of NETs. In individuals with impaired NETosis, MSU crystals induce uncontrolled production of inflammatory mediators from neutrophils and persistent inflammation. Furthermore, in models of neutrophilic inflammation, NETosis-deficient mice develop exacerbated and chronic disease that can be reduced by adoptive transfer of aggregated NETs. These findings suggest that aggregated NETs promote the resolution of neutrophilic inflammation by degrading cytokines and chemokines and disrupting neutrophil recruitment and activation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schauer</LastName><ForeName>Christine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Janko</LastName><ForeName>Christina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>1] Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany. [2] Department of Otorhinolaryngology, Head and Neck Surgery, Section for Experimental Oncology and Nanomedicine (SEON), University Hospital Erlangen, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Munoz</LastName><ForeName>Luis E</ForeName><Initials>LE</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Yi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>1] Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany. [2] Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kienhöfer</LastName><ForeName>Deborah</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frey</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology, University Hospital Erlangen, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lell</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Radiology, Friedrich-Alexander University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manger</LastName><ForeName>Bernhard</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rech</LastName><ForeName>Jürgen</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Naschberger</LastName><ForeName>Elisabeth</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Division of Molecular and Experimental Surgery, Department of Surgery, University of Erlangen Medical Center, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Holmdahl</LastName><ForeName>Rikard</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Division of Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krenn</LastName><ForeName>Veit</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Department of Pathology, MVZ of Pathology, Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Harrer</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jeremic</LastName><ForeName>Ivica</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>1] Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany. [2] Institute of Rheumatology, School of Medicine, University of Belgrade, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bilyy</LastName><ForeName>Rostyslav</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Institute of Cell Biology, National Academy of Sciences of Ukraine, Lviv, Ukraine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schett</LastName><ForeName>Georg</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hoffmann</LastName><ForeName>Markus</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Herrmann</LastName><ForeName>Martin</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>04</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Nat Med</MedlineTA><NlmUniqueID>9502015</NlmUniqueID><ISSNLinking>1078-8956</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018925">Chemokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016897" MajorTopicYN="N">Respiratory Burst</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013582" MajorTopicYN="N">Synovial Fluid</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014527" MajorTopicYN="N">Uric Acid</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>12</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>03</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>5</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>5</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>6</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24784231</ArticleId><ArticleId IdType="pii">nm.3547</ArticleId><ArticleId IdType="doi">10.1038/nm.3547</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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