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Auranofin inhibits the induction of interleukin 1beta and tumor necrosis factor alpha mRNA in macrophages

Bondeson, J and Sundler, Roger LU (1995) In Biochemical Pharmacology 50(11). p.9-1753
Abstract
Gold compounds are widely used in the treatment of rheumatoid arthritis, but their mechanisms of action remain unclear. We demonstrate here that auranofin (AF) (0.1-3 microM), but neither the hydrophilic gold compounds aurothiomalate (ATM) and aurothioglucose nor methotrexate or D-penicillamine, inhibits the induction of interleukin 1 beta and tumor necrosis factor (TNF) alpha mRNA and protein by either zymosan, lipopolysaccharide (LPS), or various bacteria in mouse macrophages. The auranofin-mediated inhibition of the induction of TNF-alpha mRNA was stronger than that of interleukin (IL) 1 beta mRNA. AF, but not the other drugs, also inhibited zymosan-induced mobilization of arachidonate. The fact that AF inhibited the induction of mRNA... (More)
Gold compounds are widely used in the treatment of rheumatoid arthritis, but their mechanisms of action remain unclear. We demonstrate here that auranofin (AF) (0.1-3 microM), but neither the hydrophilic gold compounds aurothiomalate (ATM) and aurothioglucose nor methotrexate or D-penicillamine, inhibits the induction of interleukin 1 beta and tumor necrosis factor (TNF) alpha mRNA and protein by either zymosan, lipopolysaccharide (LPS), or various bacteria in mouse macrophages. The auranofin-mediated inhibition of the induction of TNF-alpha mRNA was stronger than that of interleukin (IL) 1 beta mRNA. AF, but not the other drugs, also inhibited zymosan-induced mobilization of arachidonate. The fact that AF inhibited the induction of mRNA for both these proinflammatory cytokines, irrespective of which stimulus was used, may indicate that it affects some common signal transduction step vital to their induction. (Less)
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type
Contribution to journal
publication status
published
subject
in
Biochemical Pharmacology
volume
50
issue
11
pages
9 - 1753
publisher
Elsevier
external identifiers
  • scopus:0029589336
ISSN
0006-2952
language
English
LU publication?
yes
id
596a7997-83ca-4c35-bb4a-51cd79a23cea (old id 30112)
date added to LUP
2016-04-01 12:28:22
date last changed
2021-05-02 04:04:52
@article{596a7997-83ca-4c35-bb4a-51cd79a23cea,
  abstract     = {{Gold compounds are widely used in the treatment of rheumatoid arthritis, but their mechanisms of action remain unclear. We demonstrate here that auranofin (AF) (0.1-3 microM), but neither the hydrophilic gold compounds aurothiomalate (ATM) and aurothioglucose nor methotrexate or D-penicillamine, inhibits the induction of interleukin 1 beta and tumor necrosis factor (TNF) alpha mRNA and protein by either zymosan, lipopolysaccharide (LPS), or various bacteria in mouse macrophages. The auranofin-mediated inhibition of the induction of TNF-alpha mRNA was stronger than that of interleukin (IL) 1 beta mRNA. AF, but not the other drugs, also inhibited zymosan-induced mobilization of arachidonate. The fact that AF inhibited the induction of mRNA for both these proinflammatory cytokines, irrespective of which stimulus was used, may indicate that it affects some common signal transduction step vital to their induction.}},
  author       = {{Bondeson, J and Sundler, Roger}},
  issn         = {{0006-2952}},
  language     = {{eng}},
  number       = {{11}},
  pages        = {{9--1753}},
  publisher    = {{Elsevier}},
  series       = {{Biochemical Pharmacology}},
  title        = {{Auranofin inhibits the induction of interleukin 1beta and tumor necrosis factor alpha mRNA in macrophages}},
  volume       = {{50}},
  year         = {{1995}},
}