{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T03:34:27Z","timestamp":1761708867443,"version":"3.37.3"},"reference-count":37,"publisher":"Wiley","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/100000980","name":"Arthritis Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000980","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2013]]},"abstract":"<jats:p>Prostaglandin (PG)D<jats:sub>2<\/jats:sub>has been shown to be an active agent in the resolution of experimentally induced inflammation. This study was undertaken to determine the presence of PGD<jats:sub>2<\/jats:sub>in chronic joint effusions and to explore the potential contributions of dendritic cells (DC) and monocytes to the intra-articular synthesis of PGD<jats:sub>2<\/jats:sub>. Synovial fluid (SF) was obtained from patients with inflammatory arthritis and knee effusions. PGD<jats:sub>2<\/jats:sub>and PGE<jats:sub>2<\/jats:sub>were detected in SF by ultrahigh-performance tandem mass spectrometry. Cellular fractions in SF were separated by density-gradient centrifugation and flow cytometry. The expression of hematopoietic prostaglandin D-synthase (hPGDS) and PGE-synthase (PGES) mRNA was determined by RT-PCR. Both PGD<jats:sub>2<\/jats:sub>and PGE<jats:sub>2<\/jats:sub>were detected in blood and SF, with PGD<jats:sub>2<\/jats:sub>being more abundant than PGE<jats:sub>2<\/jats:sub>in SF. mRNA for hPGDS was more abundant in SF mDCs than SF monocytes (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.01<\/mml:mn><\/mml:mrow><\/mml:math>) or PB monocytes (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.001<\/mml:mn><\/mml:mrow><\/mml:math>). SF mDC expressed significantly more hPGDS than PGES. Expressions of PGD<jats:sub>2<\/jats:sub>and hPGDS were inversely associated with serum C-reactive protein (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.01<\/mml:mn><\/mml:mrow><\/mml:math>) and erythrocyte sedimentation rate (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.01<\/mml:mn><\/mml:mrow><\/mml:math>). The findings suggest that synovial DCs may be an important source of hPGDS and that systemic disease activity may be influenced by actions of PGD<jats:sub>2<\/jats:sub>in RA and other arthropathies.<\/jats:p>","DOI":"10.1155\/2013\/329494","type":"journal-article","created":{"date-parts":[[2013,5,8]],"date-time":"2013-05-08T00:36:12Z","timestamp":1367973372000},"page":"1-8","source":"Crossref","is-referenced-by-count":12,"title":["Prostaglandin D<sub><b>2<\/b><\/sub>in Inflammatory Arthritis and Its Relation with Synovial Fluid Dendritic Cells"],"prefix":"10.1155","volume":"2013","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0806-1727","authenticated-orcid":true,"given":"Mahin","family":"Moghaddami","sequence":"first","affiliation":[{"name":"Arthritis Research Laboratory, Hanson Institute, SA Pathology, Adelaide, SA 5000, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Enzo","family":"Ranieri","sequence":"additional","affiliation":[{"name":"Genetics and Molecular Pathology, Women\u2019s & Children\u2019s Hospital Campus, North Adelaide, SA 5006, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael","family":"James","sequence":"additional","affiliation":[{"name":"Arthritis Research Laboratory, Hanson Institute, SA Pathology, Adelaide, SA 5000, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Janice","family":"Fletcher","sequence":"additional","affiliation":[{"name":"Genetics and Molecular Pathology, Women\u2019s & Children\u2019s Hospital Campus, North Adelaide, SA 5006, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leslie G.","family":"Cleland","sequence":"additional","affiliation":[{"name":"Arthritis Research Laboratory, Hanson Institute, SA Pathology, Adelaide, SA 5000, Australia"},{"name":"Rheumatology Unit, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","reference":[{"key":"1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tibs.2007.09.013"},{"key":"2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1332766100"},{"key":"3","doi-asserted-by":"crossref","first-page":"S78","DOI":"10.1007\/s000110050284","volume":"47","year":"1998","journal-title":"Inflammation 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