[Histopathophysiology of Gout].
Identifieur interne : 000190 ( PubMed/Curation ); précédent : 000189; suivant : 000191[Histopathophysiology of Gout].
Auteurs : Thomas Hügle ; Veit Krenn [Allemagne]Source :
- Therapeutische Umschau. Revue therapeutique [ 0040-5930 ] ; 2016.
English descriptors
- KwdEn :
- Arthritis, Gouty (pathology), Arthritis, Gouty (physiopathology), Humans, Hyperplasia, Interleukin-1 (blood), Interleukin-10 (blood), Lymphocyte Activation (physiology), Lymphocytes (pathology), Lymphocytes (physiology), Neutrophils (pathology), Neutrophils (physiology), Osteoclasts (pathology), Osteoclasts (physiology), Receptors, Tumor Necrosis Factor (physiology), Synovial Membrane (pathology), Synovial Membrane (physiopathology), Tumor Necrosis Factor-alpha (metabolism), Uric Acid (blood).
- MESH :
- chemical , blood : Interleukin-1, Interleukin-10, Uric Acid.
- chemical , metabolism : Tumor Necrosis Factor-alpha.
- pathology : Arthritis, Gouty, Lymphocytes, Neutrophils, Osteoclasts, Synovial Membrane.
- physiology : Lymphocyte Activation, Lymphocytes, Neutrophils, Osteoclasts, Receptors, Tumor Necrosis Factor.
- physiopathology : Arthritis, Gouty, Synovial Membrane.
- Humans, Hyperplasia.
Abstract
Despite being a frequent cause of arthritis and bone erosions, the underlying cellular and subcellular reaction in gout is insufficiently understood. The inflammasome as intracellular sensor for crystals plays an important role, notably resulting in interleukin (IL)-1 production. Morphologically, hyperplasia of the synovial membrane with joint effusion, along with fibrinogen deposition and influx of neutrophils and lymphocytes are observed. Extracellular NET formation by neutrophils is involved in the regulation of inflammatory tissue reaction. Furthermore, the release of IL-10 and tumor necrosis factor (TNF)-receptors along with lymphocyte proliferation induce the natural resolution of acute gouty arthritis which typically occurs after several days. In contrast to acute gout, tophi consisting of urate crystals are surrounded by histiocytes and multinucleated cells, resembling a foreign body reaction. The deposition of extracellular matrix by fibrocytes is usually observed around tophi. This fibrotic reaction is likely enhanced by Th2-lymphocytes. Bone erosions in gout occur around tophi and are triggered by osteoclast activation through RANK-ligand expression by lymphocytes. In conclusion, understanding the orchestration of inflammation in gout might help to identify new therapeutic targets.
DOI: 10.1024/0040-5930/a000769
PubMed: 27008445
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Thomas Hügle<affiliation><nlm:affiliation>1 Abteilung Rheumatologie, Universitätsspital Basel.</nlm:affiliation><wicri:noCountry code="subField">Universitätsspital Basel</wicri:noCountry></affiliation>Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">[Histopathophysiology of Gout].</title><author><name sortKey="Hugle, Thomas" sort="Hugle, Thomas" uniqKey="Hugle T" first="Thomas" last="Hügle">Thomas Hügle</name><affiliation><nlm:affiliation>1 Abteilung Rheumatologie, Universitätsspital Basel.</nlm:affiliation><wicri:noCountry code="subField">Universitätsspital Basel</wicri:noCountry></affiliation></author><author><name sortKey="Krenn, Veit" sort="Krenn, Veit" uniqKey="Krenn V" first="Veit" last="Krenn">Veit Krenn</name><affiliation wicri:level="1"><nlm:affiliation>2 MVZ-Zentrum für Histologie, Zytologie und Molekulare Diagnostik, Trier, Deutschland.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>2 MVZ-Zentrum für Histologie, Zytologie und Molekulare Diagnostik, Trier</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27008445</idno><idno type="pmid">27008445</idno><idno type="doi">10.1024/0040-5930/a000769</idno><idno type="wicri:Area/PubMed/Corpus">000190</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000190</idno><idno type="wicri:Area/PubMed/Curation">000190</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000190</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">[Histopathophysiology of Gout].</title><author><name sortKey="Hugle, Thomas" sort="Hugle, Thomas" uniqKey="Hugle T" first="Thomas" last="Hügle">Thomas Hügle</name><affiliation><nlm:affiliation>1 Abteilung Rheumatologie, Universitätsspital Basel.</nlm:affiliation><wicri:noCountry code="subField">Universitätsspital Basel</wicri:noCountry></affiliation></author><author><name sortKey="Krenn, Veit" sort="Krenn, Veit" uniqKey="Krenn V" first="Veit" last="Krenn">Veit Krenn</name><affiliation wicri:level="1"><nlm:affiliation>2 MVZ-Zentrum für Histologie, Zytologie und Molekulare Diagnostik, Trier, Deutschland.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>2 MVZ-Zentrum für Histologie, Zytologie und Molekulare Diagnostik, Trier</wicri:regionArea></affiliation></author></analytic><series><title level="j">Therapeutische Umschau. Revue therapeutique</title><idno type="ISSN">0040-5930</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Arthritis, Gouty (pathology)</term><term>Arthritis, Gouty (physiopathology)</term><term>Humans</term><term>Hyperplasia</term><term>Interleukin-1 (blood)</term><term>Interleukin-10 (blood)</term><term>Lymphocyte Activation (physiology)</term><term>Lymphocytes (pathology)</term><term>Lymphocytes (physiology)</term><term>Neutrophils (pathology)</term><term>Neutrophils (physiology)</term><term>Osteoclasts (pathology)</term><term>Osteoclasts (physiology)</term><term>Receptors, Tumor Necrosis Factor (physiology)</term><term>Synovial Membrane (pathology)</term><term>Synovial Membrane (physiopathology)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term><term>Uric Acid (blood)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Interleukin-1</term><term>Interleukin-10</term><term>Uric Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Arthritis, Gouty</term><term>Lymphocytes</term><term>Neutrophils</term><term>Osteoclasts</term><term>Synovial Membrane</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphocyte Activation</term><term>Lymphocytes</term><term>Neutrophils</term><term>Osteoclasts</term><term>Receptors, Tumor Necrosis Factor</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Arthritis, Gouty</term><term>Synovial Membrane</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Hyperplasia</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Despite being a frequent cause of arthritis and bone erosions, the underlying cellular and subcellular reaction in gout is insufficiently understood. The inflammasome as intracellular sensor for crystals plays an important role, notably resulting in interleukin (IL)-1 production. Morphologically, hyperplasia of the synovial membrane with joint effusion, along with fibrinogen deposition and influx of neutrophils and lymphocytes are observed. Extracellular NET formation by neutrophils is involved in the regulation of inflammatory tissue reaction. Furthermore, the release of IL-10 and tumor necrosis factor (TNF)-receptors along with lymphocyte proliferation induce the natural resolution of acute gouty arthritis which typically occurs after several days. In contrast to acute gout, tophi consisting of urate crystals are surrounded by histiocytes and multinucleated cells, resembling a foreign body reaction. The deposition of extracellular matrix by fibrocytes is usually observed around tophi. This fibrotic reaction is likely enhanced by Th2-lymphocytes. Bone erosions in gout occur around tophi and are triggered by osteoclast activation through RANK-ligand expression by lymphocytes. In conclusion, understanding the orchestration of inflammation in gout might help to identify new therapeutic targets.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27008445</PMID><DateCreated><Year>2016</Year><Month>03</Month><Day>24</Day></DateCreated><DateCompleted><Year>2016</Year><Month>07</Month><Day>12</Day></DateCompleted><DateRevised><Year>2016</Year><Month>03</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0040-5930</ISSN><JournalIssue CitedMedium="Print"><Volume>73</Volume><Issue>3</Issue><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>Therapeutische Umschau. Revue therapeutique</Title><ISOAbbreviation>Ther Umsch</ISOAbbreviation></Journal><ArticleTitle>[Histopathophysiology of Gout].</ArticleTitle><Pagination><MedlinePgn>137-40</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1024/0040-5930/a000769</ELocationID><Abstract><AbstractText>Despite being a frequent cause of arthritis and bone erosions, the underlying cellular and subcellular reaction in gout is insufficiently understood. The inflammasome as intracellular sensor for crystals plays an important role, notably resulting in interleukin (IL)-1 production. Morphologically, hyperplasia of the synovial membrane with joint effusion, along with fibrinogen deposition and influx of neutrophils and lymphocytes are observed. Extracellular NET formation by neutrophils is involved in the regulation of inflammatory tissue reaction. Furthermore, the release of IL-10 and tumor necrosis factor (TNF)-receptors along with lymphocyte proliferation induce the natural resolution of acute gouty arthritis which typically occurs after several days. In contrast to acute gout, tophi consisting of urate crystals are surrounded by histiocytes and multinucleated cells, resembling a foreign body reaction. The deposition of extracellular matrix by fibrocytes is usually observed around tophi. This fibrotic reaction is likely enhanced by Th2-lymphocytes. Bone erosions in gout occur around tophi and are triggered by osteoclast activation through RANK-ligand expression by lymphocytes. In conclusion, understanding the orchestration of inflammation in gout might help to identify new therapeutic targets.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hügle</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>1 Abteilung Rheumatologie, Universitätsspital Basel.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krenn</LastName><ForeName>Veit</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>2 MVZ-Zentrum für Histologie, Zytologie und Molekulare Diagnostik, Trier, Deutschland.</Affiliation></AffiliationInfo></Author></AuthorList><Language>ger</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>Histo-Pathophysiologie der Gichtarthritis.</VernacularTitle></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Ther Umsch</MedlineTA><NlmUniqueID>0407224</NlmUniqueID><ISSNLinking>0040-5930</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007375">Interleukin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018124">Receptors, Tumor Necrosis Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>130068-27-8</RegistryNumber><NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance></Chemical><Chemical><RegistryNumber>268B43MJ25</RegistryNumber><NameOfSubstance UI="D014527">Uric Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015210" MajorTopicYN="N">Arthritis, Gouty</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006965" MajorTopicYN="N">Hyperplasia</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007375" MajorTopicYN="N">Interleukin-1</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016753" MajorTopicYN="N">Interleukin-10</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008213" MajorTopicYN="N">Lymphocyte Activation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008214" MajorTopicYN="N">Lymphocytes</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009504" MajorTopicYN="N">Neutrophils</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010010" MajorTopicYN="N">Osteoclasts</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018124" MajorTopicYN="N">Receptors, Tumor Necrosis Factor</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013583" MajorTopicYN="N">Synovial Membrane</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014527" MajorTopicYN="N">Uric Acid</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>3</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>3</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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