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Mechanism of action of disease modifying anti-rheumatic agent, gold sodium thiomalate (GSTM).

Abstract：

:GSTM has been used for long in the treatment of rheumatoid arthritis (RA). However, its mechanism of action is still poorly understood. In the last decade, tumor necrosis factor-alpha (TNF-alpha) has emerged as the major pro-inflammatory cytokine in the pathogenesis of RA. We studied the effect of GSTM on spontaneous and LPS-stimulated TNF-alpha production by human peripheral blood mononuclear cells (PBMCs) of normal volunteers. PBMCs were isolated from 20 normal volunteers and cultured in the presence of absence of lipopolysaccharide (LPS 10 ng/ml) and GSTM (1 microgram/ml). TNF-alpha level was measured using commercial enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). The TNF-alpha response to LPS was heterogeneous. PBMCs of 24 subjects showed high LPS-stimulated TNF-alpha production (LPS-responsive group), whereas that of six individuals had low LPS-stimulated TNF-alpha production (LPS-non-responsive group). GSTM-stimulated spontaneous TNF-alpha production and inhibited LPS-stimulated TNF-alpha production in 16 of 24 (75%) individuals of LPS-responsive group and one of six individuals (17%) of LPS-non-responsive group. The suppression of TNF-alpha by GSTM was also demonstrated at the mRNA level. We conclude that there is a heterogeneity among normal population for TNF-alpha production in response to LPS, and GSTM inhibits LPS-stimulated TNF-alpha production, primarily in LPS responders. Further study is needed to establish the relationship between LPS responsiveness and GSTM suppression.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Mangalam AK,Aggarwal A,Naik S

doi

10.1016/s1567-5769(01)00050-9

keywords:

subject

Has Abstract

pub_date

2001-06-01 00:00:00

pages

1165-72

issue

6

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(01)00050-9

journal_volume

1

pub_type

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