PMID- 9263137
OWN - NLM
STAT- MEDLINE
DCOM- 19970925
LR  - 20131121
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 24
IP  - 8
DP  - 1997 Aug
TI  - In vitro modulation of cytokine, cytokine inhibitor, and prostaglandin E release 
      from blood mononuclear cells and synovial fibroblasts by antirheumatic drugs.
PG  - 1471-6
AB  - OBJECTIVE: To assess the effect of various antirheumatic drugs on cytokine, 
      cytokine inhibitor, and prostaglandin E (PGE) production by normal blood 
      mononuclear cells (MNC) and rheumatoid arthritis (RA) synovial fibroblasts in 
      vitro. METHODS: MNC from healthy donors and RA synovial fibroblasts were 
      preincubated with or without prostaglandin E2 (PGE2), indomethacin, 
      dexamethasone, gold sodium thiomalate (GSTM), methotrexate (MTX), and cyclosporin 
      A (CyA), and then cultured in the absence or presence of interleukin-1 beta (IL-1 
      beta) or tumor necrosis factor-alpha (TNF-alpha) for 48 h. We characterized 
      cytokines such as IL-1 beta, IL-8, monocyte chemoattractant protein-1 (MCP-1), 
      and cytokine inhibitors such as IL-1 receptor antagonist (IL-1ra) and soluble TNF 
      receptors (sTNFR p55 + p75) as well as PGE in the cell-free culture supernatants. 
      RESULTS: In MNC and synovial fibroblast cultures dexamethasone, GSTM, and PGE2 
      most markedly downregulated spontaneous and/or cytokine stimulated production of 
      IL-1 beta, IL-14a, IL-8, and MCP-1, whereas sTNFR shedding was not affected. In 
      contrast, MTX and CyA had only marginal or no effects on mediator release, 
      whereas indomethacin inhibited only PGE production. CONCLUSION: Among several 
      antirheumatic drugs examined, dexamethasone and GSTM exhibited the most potent 
      inhibitory effects on inflammatory cytokine and cytokine inhibitor production by 
      blood mononuclear cells and synovial fibroblasts. These drugs may exert their 
      antiinflammatory actions by unspecific suppression of monocyte and fibroblast 
      secretory function.
FAU - Seitz, M
AU  - Seitz M
AD  - Department of Rheumatology, University Hospital, Berne, Switzerland.
FAU - Loetscher, P
AU  - Loetscher P
FAU - Dewald, B
AU  - Dewald B
FAU - Towbin, H
AU  - Towbin H
FAU - Baggiolini, M
AU  - Baggiolini M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Cytokines)
RN  - 0 (IL1RN protein, human)
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Sialoglycoproteins)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Antirheumatic Agents/*pharmacology
MH  - Arthritis, Rheumatoid/drug therapy/pathology
MH  - Cells, Cultured
MH  - Cytokines/antagonists & inhibitors/*metabolism/pharmacology
MH  - Dinoprostone/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Down-Regulation
MH  - Fibroblasts/drug effects/*metabolism
MH  - Humans
MH  - Interleukin 1 Receptor Antagonist Protein
MH  - Leukocytes, Mononuclear/drug effects/*metabolism
MH  - Receptors, Tumor Necrosis Factor/*metabolism
MH  - Sialoglycoproteins/*metabolism
MH  - Synovial Membrane/pathology
EDAT- 1997/08/01 00:00
MHDA- 1997/08/01 00:01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/08/01 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
PST - ppublish
SO  - J Rheumatol. 1997 Aug;24(8):1471-6.