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Alterations in human monocyte structure and function induced by incubation with gold sodium thiomalate
The Journal of Rheumatology. Supplement
|January 1, 1979
Summary
Gold sodium thiomalate (GST) causes vacuole formation and impairs the phagocytic functions of human mononuclear phagocytes (Mphi). This suggests GST
Area of Science:
- Immunology
- Pharmacology
- Cell Biology
Background:
- Rheumatoid arthritis is a chronic inflammatory disease.
- Mononuclear phagocytes (Mphi) play a key role in immune responses and inflammation.
- Gold sodium thiomalate (GST) is a disease-modifying antirheumatic drug used in rheumatoid arthritis treatment.
Purpose of the Study:
- To investigate the in vitro effects of gold sodium thiomalate (GST) on the morphology and function of human mononuclear phagocytes (Mphi).
- To elucidate the cellular mechanisms underlying GST's therapeutic action in rheumatoid arthritis.
Main Methods:
- Human peripheral blood Mphi were incubated with GST (25 µg/ml) for 4 days.
- Morphological changes were assessed by microscopy.
- Functional assays included measurement of glass adherence, Fc receptor-mediated particle binding, pinocytosis of horseradish peroxidase, and phagocytosis of IgG-opsonized erythrocytes.
Main Results:
- GST incubation led to the development of large intracytoplasmic vacuoles in Mphi.
- Similar vacuolization was observed with gold chloride but not thiomalic acid.
- GST significantly diminished Mphi pinocytosis and phagocytosis, while having minimal effect on adherence and Fc receptor binding.
Conclusions:
- Gold sodium thiomalate induces significant morphological and functional alterations in human mononuclear phagocytes.
- The observed effects on Mphi function, particularly reduced phagocytosis, may contribute to the therapeutic efficacy of GST in rheumatoid arthritis.
- GST's mechanism of action may involve modulating the functional capacity of Mphi.