IL-33 enhances macrophage release of IL-1β and promotes pain and inflammation in gouty arthritis
Objective To investigate the role of IL-33 in gouty arthritis. Material 174 Balb/c (wild-type) and 54 ST2 −/− mice were used in this study. In vitro experiments were conducted in bone marrow-derived macrophages (BMDMs). Synovial fluid samples from gouty arthritis ( n = 7) and osteoarthritis ( n = ...
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| Veröffentlicht in: | Inflammation research 2020-12, Vol.69 (12), p.1271-1282 |
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| creator | Fattori, Victor Staurengo-Ferrari, Larissa Zaninelli, Tiago H. Casagrande, Rubia Oliveira, Rene D. Louzada-Junior, Paulo Cunha, Thiago M. Alves-Filho, Jose C. Teixeira, Mauro M. Cunha, Fernando Q. Amaral, Flavio A. Verri, Waldiceu A. |
| description | Objective
To investigate the role of IL-33 in gouty arthritis.
Material
174 Balb/c (wild-type) and 54 ST2
−/−
mice were used in this study. In vitro experiments were conducted in bone marrow-derived macrophages (BMDMs). Synovial fluid samples from gouty arthritis (
n
= 7) and osteoarthritis (
n
= 8) hospital patients were used to measure IL-33 and sST2 levels.
Methods
Gout was induced by injection of monosodium urate (MSU) crystals in the knee joint of mice. Pain was determined using the electronic von Frey and static weight bearing. Neutrophil recruitment was determined by H&E staining, Rosenfeld staining slides, and MPO activity. ELISA was used for cytokine and sST2 measurement. The priming effect of IL-33 was determined in BMDM.
Results
Synovial fluid of gout patients showed higher IL-33 levels and neutrophil counts than osteoarthritis patients. In mice, the absence of ST2 prevented mechanical pain, knee joint edema, neutrophil recruitment to the knee joint, and lowered IL-1β and superoxide anion levels. In macrophages, IL-33 enhanced the release of IL-1β and TNF-α, and BMDMs from ST2
−/−
showed reduced levels of these cytokines after stimulus with MSU crystals.
Conclusion
IL-33 mediates gout pain and inflammation by boosting macrophages production of cytokines upon MSU crystals stimulus. |
| doi_str_mv | 10.1007/s00011-020-01399-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2471680305</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2471680305</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-da1e9cacd042337700908545ccd823738dcc105892ef2505a3303d02d820dadd3</originalsourceid><addsrcrecordid>eNp9kEtOwzAQhi0EoqVwARbIEmvD2JM0zhJVPCpVYgMSO8vYTpuqeWAnUnstDsKZMA2PHauZ8Xzzj-cn5JzDFQfIrgMAcM5AAAOOec62B2TMk1jmIF8OYw4CGUqEETkJYR1xKaQ4JiMUUk55Mh0TPV8wROrqla6NC7TSxjftSi8d9W7jdHC0KWiE-Mc71bWlrW-qpotkq8t6_1LWxUZXle7Kpo4FXTZ9t6PadytfdmU4JUeF3gR39h0n5Pnu9mn2wBaP9_PZzYIZzNKOWc1dbrSxkAjELAOIR6RJaoyVAjOU1hgOqcyFK0QKqUYEtCBiF6y2FifkctCNP3zrXejUuul9HVcqkWR8KgEhjZQYqHhmCN4VqvVlpf1OcVBfrqrBVRVdVXtX1TYOXXxL96-Vs78jPzZGAAcgxFa9dP5v9z-yn6Q-gns</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2471680305</pqid></control><display><type>article</type><title>IL-33 enhances macrophage release of IL-1β and promotes pain and inflammation in gouty arthritis</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Fattori, Victor ; Staurengo-Ferrari, Larissa ; Zaninelli, Tiago H. ; Casagrande, Rubia ; Oliveira, Rene D. ; Louzada-Junior, Paulo ; Cunha, Thiago M. ; Alves-Filho, Jose C. ; Teixeira, Mauro M. ; Cunha, Fernando Q. ; Amaral, Flavio A. ; Verri, Waldiceu A.</creator><creatorcontrib>Fattori, Victor ; Staurengo-Ferrari, Larissa ; Zaninelli, Tiago H. ; Casagrande, Rubia ; Oliveira, Rene D. ; Louzada-Junior, Paulo ; Cunha, Thiago M. ; Alves-Filho, Jose C. ; Teixeira, Mauro M. ; Cunha, Fernando Q. ; Amaral, Flavio A. ; Verri, Waldiceu A.</creatorcontrib><description>Objective
To investigate the role of IL-33 in gouty arthritis.
Material
174 Balb/c (wild-type) and 54 ST2
−/−
mice were used in this study. In vitro experiments were conducted in bone marrow-derived macrophages (BMDMs). Synovial fluid samples from gouty arthritis (
n
= 7) and osteoarthritis (
n
= 8) hospital patients were used to measure IL-33 and sST2 levels.
Methods
Gout was induced by injection of monosodium urate (MSU) crystals in the knee joint of mice. Pain was determined using the electronic von Frey and static weight bearing. Neutrophil recruitment was determined by H&E staining, Rosenfeld staining slides, and MPO activity. ELISA was used for cytokine and sST2 measurement. The priming effect of IL-33 was determined in BMDM.
Results
Synovial fluid of gout patients showed higher IL-33 levels and neutrophil counts than osteoarthritis patients. In mice, the absence of ST2 prevented mechanical pain, knee joint edema, neutrophil recruitment to the knee joint, and lowered IL-1β and superoxide anion levels. In macrophages, IL-33 enhanced the release of IL-1β and TNF-α, and BMDMs from ST2
−/−
showed reduced levels of these cytokines after stimulus with MSU crystals.
Conclusion
IL-33 mediates gout pain and inflammation by boosting macrophages production of cytokines upon MSU crystals stimulus.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-020-01399-x</identifier><identifier>PMID: 32886146</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Allergology ; Animals ; Arthritis ; Arthritis, Gouty - chemically induced ; Arthritis, Gouty - metabolism ; Arthritis, Gouty - pathology ; Biomedical and Life Sciences ; Biomedical materials ; Biomedicine ; Bone marrow ; Crystals ; Cytokines ; Dermatology ; Edema ; Female ; Gout ; Humans ; IL-1β ; Immunology ; Inflammation - chemically induced ; Inflammation - psychology ; Interleukin-1 Receptor-Like 1 Protein - genetics ; Interleukin-1beta - metabolism ; Interleukin-33 - pharmacology ; Joints (anatomy) ; Knee ; Macrophages ; Macrophages - drug effects ; Macrophages - metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Middle Aged ; Neurology ; Neutrophil Infiltration - drug effects ; Neutrophils ; Original Research Paper ; Osteoarthritis ; Pain ; Pain - chemically induced ; Pain - psychology ; Peroxidase - metabolism ; Pharmacology/Toxicology ; Priming ; Recruitment ; Rheumatism ; Rheumatology ; Staining ; Superoxide anions ; Superoxides - metabolism ; Synovial fluid ; Synovial Membrane - pathology ; Tumor necrosis factor-α ; Uric Acid</subject><ispartof>Inflammation research, 2020-12, Vol.69 (12), p.1271-1282</ispartof><rights>Springer Nature Switzerland AG 2020</rights><rights>Springer Nature Switzerland AG 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-da1e9cacd042337700908545ccd823738dcc105892ef2505a3303d02d820dadd3</citedby><cites>FETCH-LOGICAL-c375t-da1e9cacd042337700908545ccd823738dcc105892ef2505a3303d02d820dadd3</cites><orcidid>0000-0003-2756-9283</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00011-020-01399-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00011-020-01399-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32886146$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fattori, Victor</creatorcontrib><creatorcontrib>Staurengo-Ferrari, Larissa</creatorcontrib><creatorcontrib>Zaninelli, Tiago H.</creatorcontrib><creatorcontrib>Casagrande, Rubia</creatorcontrib><creatorcontrib>Oliveira, Rene D.</creatorcontrib><creatorcontrib>Louzada-Junior, Paulo</creatorcontrib><creatorcontrib>Cunha, Thiago M.</creatorcontrib><creatorcontrib>Alves-Filho, Jose C.</creatorcontrib><creatorcontrib>Teixeira, Mauro M.</creatorcontrib><creatorcontrib>Cunha, Fernando Q.</creatorcontrib><creatorcontrib>Amaral, Flavio A.</creatorcontrib><creatorcontrib>Verri, Waldiceu A.</creatorcontrib><title>IL-33 enhances macrophage release of IL-1β and promotes pain and inflammation in gouty arthritis</title><title>Inflammation research</title><addtitle>Inflamm. Res</addtitle><addtitle>Inflamm Res</addtitle><description>Objective
To investigate the role of IL-33 in gouty arthritis.
Material
174 Balb/c (wild-type) and 54 ST2
−/−
mice were used in this study. In vitro experiments were conducted in bone marrow-derived macrophages (BMDMs). Synovial fluid samples from gouty arthritis (
n
= 7) and osteoarthritis (
n
= 8) hospital patients were used to measure IL-33 and sST2 levels.
Methods
Gout was induced by injection of monosodium urate (MSU) crystals in the knee joint of mice. Pain was determined using the electronic von Frey and static weight bearing. Neutrophil recruitment was determined by H&E staining, Rosenfeld staining slides, and MPO activity. ELISA was used for cytokine and sST2 measurement. The priming effect of IL-33 was determined in BMDM.
Results
Synovial fluid of gout patients showed higher IL-33 levels and neutrophil counts than osteoarthritis patients. In mice, the absence of ST2 prevented mechanical pain, knee joint edema, neutrophil recruitment to the knee joint, and lowered IL-1β and superoxide anion levels. In macrophages, IL-33 enhanced the release of IL-1β and TNF-α, and BMDMs from ST2
−/−
showed reduced levels of these cytokines after stimulus with MSU crystals.
Conclusion
IL-33 mediates gout pain and inflammation by boosting macrophages production of cytokines upon MSU crystals stimulus.</description><subject>Allergology</subject><subject>Animals</subject><subject>Arthritis</subject><subject>Arthritis, Gouty - chemically induced</subject><subject>Arthritis, Gouty - metabolism</subject><subject>Arthritis, Gouty - pathology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedical materials</subject><subject>Biomedicine</subject><subject>Bone marrow</subject><subject>Crystals</subject><subject>Cytokines</subject><subject>Dermatology</subject><subject>Edema</subject><subject>Female</subject><subject>Gout</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Immunology</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - psychology</subject><subject>Interleukin-1 Receptor-Like 1 Protein - genetics</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukin-33 - pharmacology</subject><subject>Joints (anatomy)</subject><subject>Knee</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Neutrophil Infiltration - drug effects</subject><subject>Neutrophils</subject><subject>Original Research Paper</subject><subject>Osteoarthritis</subject><subject>Pain</subject><subject>Pain - chemically induced</subject><subject>Pain - psychology</subject><subject>Peroxidase - metabolism</subject><subject>Pharmacology/Toxicology</subject><subject>Priming</subject><subject>Recruitment</subject><subject>Rheumatism</subject><subject>Rheumatology</subject><subject>Staining</subject><subject>Superoxide anions</subject><subject>Superoxides - metabolism</subject><subject>Synovial fluid</subject><subject>Synovial Membrane - pathology</subject><subject>Tumor necrosis factor-α</subject><subject>Uric Acid</subject><issn>1023-3830</issn><issn>1420-908X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kEtOwzAQhi0EoqVwARbIEmvD2JM0zhJVPCpVYgMSO8vYTpuqeWAnUnstDsKZMA2PHauZ8Xzzj-cn5JzDFQfIrgMAcM5AAAOOec62B2TMk1jmIF8OYw4CGUqEETkJYR1xKaQ4JiMUUk55Mh0TPV8wROrqla6NC7TSxjftSi8d9W7jdHC0KWiE-Mc71bWlrW-qpotkq8t6_1LWxUZXle7Kpo4FXTZ9t6PadytfdmU4JUeF3gR39h0n5Pnu9mn2wBaP9_PZzYIZzNKOWc1dbrSxkAjELAOIR6RJaoyVAjOU1hgOqcyFK0QKqUYEtCBiF6y2FifkctCNP3zrXejUuul9HVcqkWR8KgEhjZQYqHhmCN4VqvVlpf1OcVBfrqrBVRVdVXtX1TYOXXxL96-Vs78jPzZGAAcgxFa9dP5v9z-yn6Q-gns</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Fattori, Victor</creator><creator>Staurengo-Ferrari, Larissa</creator><creator>Zaninelli, Tiago H.</creator><creator>Casagrande, Rubia</creator><creator>Oliveira, Rene D.</creator><creator>Louzada-Junior, Paulo</creator><creator>Cunha, Thiago M.</creator><creator>Alves-Filho, Jose C.</creator><creator>Teixeira, Mauro M.</creator><creator>Cunha, Fernando Q.</creator><creator>Amaral, Flavio A.</creator><creator>Verri, Waldiceu A.</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0003-2756-9283</orcidid></search><sort><creationdate>20201201</creationdate><title>IL-33 enhances macrophage release of IL-1β and promotes pain and inflammation in gouty arthritis</title><author>Fattori, Victor ; Staurengo-Ferrari, Larissa ; Zaninelli, Tiago H. ; Casagrande, Rubia ; Oliveira, Rene D. ; Louzada-Junior, Paulo ; Cunha, Thiago M. ; Alves-Filho, Jose C. ; Teixeira, Mauro M. ; Cunha, Fernando Q. ; Amaral, Flavio A. ; Verri, Waldiceu A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-da1e9cacd042337700908545ccd823738dcc105892ef2505a3303d02d820dadd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Allergology</topic><topic>Animals</topic><topic>Arthritis</topic><topic>Arthritis, Gouty - chemically induced</topic><topic>Arthritis, Gouty - metabolism</topic><topic>Arthritis, Gouty - pathology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedical materials</topic><topic>Biomedicine</topic><topic>Bone marrow</topic><topic>Crystals</topic><topic>Cytokines</topic><topic>Dermatology</topic><topic>Edema</topic><topic>Female</topic><topic>Gout</topic><topic>Humans</topic><topic>IL-1β</topic><topic>Immunology</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - psychology</topic><topic>Interleukin-1 Receptor-Like 1 Protein - genetics</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukin-33 - pharmacology</topic><topic>Joints (anatomy)</topic><topic>Knee</topic><topic>Macrophages</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Knockout</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Neutrophil Infiltration - drug effects</topic><topic>Neutrophils</topic><topic>Original Research Paper</topic><topic>Osteoarthritis</topic><topic>Pain</topic><topic>Pain - chemically induced</topic><topic>Pain - psychology</topic><topic>Peroxidase - metabolism</topic><topic>Pharmacology/Toxicology</topic><topic>Priming</topic><topic>Recruitment</topic><topic>Rheumatism</topic><topic>Rheumatology</topic><topic>Staining</topic><topic>Superoxide anions</topic><topic>Superoxides - metabolism</topic><topic>Synovial fluid</topic><topic>Synovial Membrane - pathology</topic><topic>Tumor necrosis factor-α</topic><topic>Uric Acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fattori, Victor</creatorcontrib><creatorcontrib>Staurengo-Ferrari, Larissa</creatorcontrib><creatorcontrib>Zaninelli, Tiago H.</creatorcontrib><creatorcontrib>Casagrande, Rubia</creatorcontrib><creatorcontrib>Oliveira, Rene D.</creatorcontrib><creatorcontrib>Louzada-Junior, Paulo</creatorcontrib><creatorcontrib>Cunha, Thiago M.</creatorcontrib><creatorcontrib>Alves-Filho, Jose C.</creatorcontrib><creatorcontrib>Teixeira, Mauro M.</creatorcontrib><creatorcontrib>Cunha, Fernando Q.</creatorcontrib><creatorcontrib>Amaral, Flavio A.</creatorcontrib><creatorcontrib>Verri, Waldiceu A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Inflammation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fattori, Victor</au><au>Staurengo-Ferrari, Larissa</au><au>Zaninelli, Tiago H.</au><au>Casagrande, Rubia</au><au>Oliveira, Rene D.</au><au>Louzada-Junior, Paulo</au><au>Cunha, Thiago M.</au><au>Alves-Filho, Jose C.</au><au>Teixeira, Mauro M.</au><au>Cunha, Fernando Q.</au><au>Amaral, Flavio A.</au><au>Verri, Waldiceu A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-33 enhances macrophage release of IL-1β and promotes pain and inflammation in gouty arthritis</atitle><jtitle>Inflammation research</jtitle><stitle>Inflamm. Res</stitle><addtitle>Inflamm Res</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>69</volume><issue>12</issue><spage>1271</spage><epage>1282</epage><pages>1271-1282</pages><issn>1023-3830</issn><eissn>1420-908X</eissn><abstract>Objective
To investigate the role of IL-33 in gouty arthritis.
Material
174 Balb/c (wild-type) and 54 ST2
−/−
mice were used in this study. In vitro experiments were conducted in bone marrow-derived macrophages (BMDMs). Synovial fluid samples from gouty arthritis (
n
= 7) and osteoarthritis (
n
= 8) hospital patients were used to measure IL-33 and sST2 levels.
Methods
Gout was induced by injection of monosodium urate (MSU) crystals in the knee joint of mice. Pain was determined using the electronic von Frey and static weight bearing. Neutrophil recruitment was determined by H&E staining, Rosenfeld staining slides, and MPO activity. ELISA was used for cytokine and sST2 measurement. The priming effect of IL-33 was determined in BMDM.
Results
Synovial fluid of gout patients showed higher IL-33 levels and neutrophil counts than osteoarthritis patients. In mice, the absence of ST2 prevented mechanical pain, knee joint edema, neutrophil recruitment to the knee joint, and lowered IL-1β and superoxide anion levels. In macrophages, IL-33 enhanced the release of IL-1β and TNF-α, and BMDMs from ST2
−/−
showed reduced levels of these cytokines after stimulus with MSU crystals.
Conclusion
IL-33 mediates gout pain and inflammation by boosting macrophages production of cytokines upon MSU crystals stimulus.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>32886146</pmid><doi>10.1007/s00011-020-01399-x</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-2756-9283</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1023-3830 |
| ispartof | Inflammation research, 2020-12, Vol.69 (12), p.1271-1282 |
| issn | 1023-3830 1420-908X |
| language | eng |
| recordid | cdi_proquest_journals_2471680305 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Allergology Animals Arthritis Arthritis, Gouty - chemically induced Arthritis, Gouty - metabolism Arthritis, Gouty - pathology Biomedical and Life Sciences Biomedical materials Biomedicine Bone marrow Crystals Cytokines Dermatology Edema Female Gout Humans IL-1β Immunology Inflammation - chemically induced Inflammation - psychology Interleukin-1 Receptor-Like 1 Protein - genetics Interleukin-1beta - metabolism Interleukin-33 - pharmacology Joints (anatomy) Knee Macrophages Macrophages - drug effects Macrophages - metabolism Male Mice Mice, Inbred BALB C Mice, Knockout Middle Aged Neurology Neutrophil Infiltration - drug effects Neutrophils Original Research Paper Osteoarthritis Pain Pain - chemically induced Pain - psychology Peroxidase - metabolism Pharmacology/Toxicology Priming Recruitment Rheumatism Rheumatology Staining Superoxide anions Superoxides - metabolism Synovial fluid Synovial Membrane - pathology Tumor necrosis factor-α Uric Acid |
| title | IL-33 enhances macrophage release of IL-1β and promotes pain and inflammation in gouty arthritis |
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