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Mediators of Inflammation
Volume 2013, Article ID 329494, 8 pages
http://dx.doi.org/10.1155/2013/329494
Research Article

Prostaglandin D2 in Inflammatory Arthritis and Its Relation with Synovial Fluid Dendritic Cells

1Arthritis Research Laboratory, Hanson Institute, SA Pathology, Adelaide, SA 5000, Australia
2Genetics and Molecular Pathology, Women’s & Children’s Hospital Campus, North Adelaide, SA 5006, Australia
3Rheumatology Unit, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia

Received 19 December 2012; Revised 18 March 2013; Accepted 10 April 2013

Academic Editor: Eric F. Morand

Copyright © 2013 Mahin Moghaddami et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Prostaglandin (PG)D2 has been shown to be an active agent in the resolution of experimentally induced inflammation. This study was undertaken to determine the presence of PGD2 in chronic joint effusions and to explore the potential contributions of dendritic cells (DC) and monocytes to the intra-articular synthesis of PGD2. Synovial fluid (SF) was obtained from patients with inflammatory arthritis and knee effusions. PGD2 and PGE2 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 PGD2 and PGE2 were detected in blood and SF, with PGD2 being more abundant than PGE2 in SF. mRNA for hPGDS was more abundant in SF mDCs than SF monocytes ( ) or PB monocytes ( ). SF mDC expressed significantly more hPGDS than PGES. Expressions of PGD2 and hPGDS were inversely associated with serum C-reactive protein ( ) and erythrocyte sedimentation rate ( ). The findings suggest that synovial DCs may be an important source of hPGDS and that systemic disease activity may be influenced by actions of PGD2 in RA and other arthropathies.