[Histopathophysiology of Gout].
Identifieur interne : 000043 ( Main/Exploration ); précédent : 000042; suivant : 000044[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
Affiliations:
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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><affiliations><list><country><li>Allemagne</li></country></list><tree><noCountry><name sortKey="Hugle, Thomas" sort="Hugle, Thomas" uniqKey="Hugle T" first="Thomas" last="Hügle">Thomas Hügle</name></noCountry><country name="Allemagne"><noRegion><name sortKey="Krenn, Veit" sort="Krenn, Veit" uniqKey="Krenn V" first="Veit" last="Krenn">Veit Krenn</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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