scholarly journals AB0206 Investigation of the inducibility of retroviruses from rheumatoid arthritis synovial fibroblasts (ra-sf) and ra-synovial fluid cells (ra-sfc)

2001 ◽  
Author(s):  
CA Seemayer ◽  
SA Kolb ◽  
J Böni ◽  
M Neidhart ◽  
B Simmen ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Synovial Fibroblasts ◽  
Synovial Fluid Cells

scholarly journals Absence of inducible retroviruses from synovial fibroblasts and synovial fluid cells of patients with rheumatoid arthritis

2002 ◽  
Vol 46 (10) ◽  
pp. 2811-2813 ◽  
Author(s):  
Christian A. Seemayer ◽  
Stefan A. Kolb ◽  
Michel Neidhart ◽  
Shiro Ohshima ◽  
Renate E. Gay ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Synovial Fibroblasts ◽  
Synovial Fluid Cells

scholarly journals RNA released from necrotic synovial fluid cells activates rheumatoid arthritis synovial fibroblasts via toll-like receptor 3

2005 ◽  
Vol 52 (9) ◽  
pp. 2656-2665 ◽  
Author(s):  
Fabia Brentano ◽  
Olivier Schorr ◽  
Renate E. Gay ◽  
Steffen Gay ◽  
Diego Kyburz
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Synovial Fibroblasts ◽  
Toll Like Receptor ◽  
Synovial Fluid Cells

scholarly journals Prostacyclin-IP signaling and prostaglandin E2-EP2/EP4 signaling both mediate joint inflammation in mouse collagen-induced arthritis

2006 ◽  
Vol 203 (2) ◽  
pp. 325-335 ◽  
Author(s):  
Tetsuya Honda ◽  
Eri Segi-Nishida ◽  
Yoshiki Miyachi ◽  
Shuh Narumiya
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Joint Inflammation ◽  
Synovial Fibroblasts ◽  
The Other ◽  
Receptor Subtype ◽  
Significant Suppression ◽  
Wild Type ◽  
Collagen Induced Arthritis

Prostaglandin (PG)I2 (prostacyclin [PGI]) and PGE2 are abundantly present in the synovial fluid of rheumatoid arthritis (RA) patients. Although the role of PGE2 in RA has been well studied, how much PGI2 contributes to RA is little known. To examine this issue, we backcrossed mice lacking the PGI receptor (IP) to the DBA/1J strain and subjected them to collagen-induced arthritis (CIA). IP-deficient (IP−/−) mice exhibited significant reduction in arthritic scores compared with wild-type (WT) mice, despite anti-collagen antibody production and complement activation similar to WT mice. IP−/− mice also showed significant reduction in contents of proinflammatory cytokines, such as interleukin (IL)-6 in arthritic paws. Consistently, the addition of an IP agonist to cultured synovial fibroblasts significantly enhanced IL-6 production and induced expression of other arthritis-related genes. On the other hand, loss or inhibition of each PGE receptor subtype alone did not affect elicitation of inflammation in CIA. However, a partial but significant suppression of CIA was achieved by the combined inhibition of EP2 and EP4. Our results show significant roles of both PGI2-IP and PGE2-EP2/EP4 signaling in the development of CIA, and suggest that inhibition of PGE2 synthesis alone may not be sufficient for suppression of RA symptoms.

scholarly journals Increased DNA and/or RNA content of synovial fluid cells in rheumatoid arthritis: a flow-cytometry study.

1984 ◽  
Vol 43 (2) ◽  
pp. 222-227 ◽  
Author(s):  
B Bonvoisin ◽  
G Cordier ◽  
J P Revillard ◽  
E Lejeune ◽  
M Bouvier
Keyword(s):  
Rheumatoid Arthritis ◽  
Flow Cytometry ◽  
Synovial Fluid ◽  
Flow Cytometry Study ◽  
Rna Content ◽  
Synovial Fluid Cells

scholarly journals Biologically active thrombomodulin is synthesized by adherent synovial fluid cells and is elevated in synovial fluid of patients with rheumatoid arthritis

Blood ◽  
1993 ◽  
Vol 81 (3) ◽  
pp. 726-733 ◽  
Author(s):  
EM Conway ◽  
B Nowakowski
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Protein C ◽  
Inflammatory Process ◽  
Biologically Active ◽  
Northern Analysis ◽  
Synovial Lining ◽  
Local Synthesis ◽  
Synovial Lining Cells ◽  
Synovial Fluid Cells

Abstract Thrombomodulin (TM) is a transmembrane glycoprotein that interacts with thrombin, thereby serving as a cofactor in the activation of protein C, a major physiologically relevant natural anticoagulant. Although initially described as a vascular endothelial cell receptor, TM has also been reported to be synthesized by several cells, including megakaryocytes, platelets, monocytes, neutrophils (PMN), mesothelial cells, and synovial lining cells. A prominent feature of rheumatoid arthritis (RA) is infiltration of PMN into the joint space. To determine whether TM might play a role in the inflammatory process, we examined synovial fluid for the presence of TM in 10 patients with RA and five patients with osteoarthritis (OA). We determined that the mean synovial fluid and plasma TM levels in the OA group were 23.5 ng/mL and 24.2 ng/mL, respectively, whereas those with RA had a significantly elevated mean synovial fluid TM level of 136.2 ng/mL as compared with the plasma TM concentration of 43.9 ng/mL (P < .05). Synovial fluid TM levels did not correlate with PMN counts (r = .261). Purified TM from synovial fluid was identical in molecular weight to plasma-derived TM and was biologically functional with respect to protein C cofactor activity. Using direct immunofluorescence, we determined that adherent cultured synovial fluid cells that are not monocytoid in origin express surface and cytoplasmic TM, thereby providing an alternative source of the protein. Biologic activity of the cell-surface TM was confirmed by acceleration of thrombin-dependent protein C activation. Northern analysis of RNA extracted from the cultured cells indicated that TM messenger RNA was present, suggesting local synthesis. Our results indicate that in RA-associated synovial effusions, biologically active TM is increased, the source of which may be from plasma, PMN, and/or synovial lining cells. TM may play a regulatory role either in fibrin deposition in the inflamed joint and/or in the progression of the inflammatory process.

scholarly journals Interleukin 34 expression is associated with synovitis severity in rheumatoid arthritis patients

2011 ◽  
Vol 71 (1) ◽  
pp. 150-154 ◽  
Author(s):  
M Chemel ◽  
B Le Goff ◽  
R Brion ◽  
C Cozic ◽  
M Berreur ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Messenger Rna ◽  
Synovial Fibroblasts ◽  
Total Leucocyte Count ◽  
Dependent Manner ◽  
Jnk Pathway ◽  
Dose Time ◽  
Downstream Effector ◽  
Factor Α

ObjectivesInterleukin (IL) 34 is a new cytokine implicated in macrophage differentiation and osteoclastogenesis. This study assessed IL-34 expression in the tissue of patients with rheumatoid arthritis (RA).MethodsImmunohistochemistry was performed in synovial biopsies from patients with RA (n=20), osteoarthritis (n=3) or other inflammatory arthritis (n=4). IL-34 was detected in the synovial fluid by ELISA and its messenger RNA expression was studied by quantitative PCR in rheumatoid synovial fibroblasts after stimulation by tumour necrosis factor α (TNFα) and IL-1β. Wild-type, jnk1−/−–jnk2−/− and nemo−/− murine fibroblasts and pharmacological inhibition were used to determine the involvement of nuclear factor kappa B (NF-κB) and JNK in that effect.ResultsIL-34 was expressed in 24/27 biopsies, with three samples from RA patients being negative. A significant association was found between IL-34 expression and synovitis severity. Levels of IL-34 and the total leucocyte count in synovial fluid were correlated. TNFα and IL-1β stimulated IL-34 expression by synovial fibroblasts in a dose/time-dependent manner through the NF-κB and JNK pathway.ConclusionThis work for the first time identifies IL-34 expression in the synovial tissue of patients with arthritis. This cytokine, as a downstream effector of TNFα and IL-1β, may contribute to inflammation and bone erosions in RA.

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