Sodium Aurothiomalate, Gold Keratinate, and Various Tetracyclines in Mycoplasma-Induced Arthritis of Rodents

Hannan, P. C. T.

doi:10.1099/00222615-10-1-87

Cited by 14 publications

(5 citation statements)

References 14 publications

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“…Furthermore, preliminary studies performed recently indicate that the same inhibitory effect is exerted by ATM on mouse lymphocyte activation by another potent mitogen, prepared from the type A strain of M. neurolyticum. Our results confirm the suggested role of ATM in the course of Mycoplasma-induced arthritis by its effect on the host's immune response (6). The extensive transformation of murine lymphocytes by various Mycoplasma mitogens (9, 10), together with the described effect of ATM on this activation, might offer an explanation of the mechanisms by which mycoplasmas induce arthritis in the infected host.…”

supporting

confidence: 85%

Inhibition of mycoplasma-induced lymphocyte activation by sodium aurothiomalate

Naot¹,

Merchav²

1978

Infect Immun

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supporting

confidence: 85%

Inhibition of mycoplasma-induced lymphocyte activation by sodium aurothiomalate

Naot¹,

Merchav²

1978

Infect Immun

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“…'5 Five different tetracycines were highly active against M arthritidis and M pulmonis induced arthritis in rodents. 16 Arthritis associated with mycoplasma infection in humans M pneumoniae infection may cause arthralgias or less commonly a migratory polyarthropathy affecting medium sized joints. This condition may be severe, with joint swelling, morning stiffness, and considerable functional disability.…”

Section: Mycoplasmal Arthritis In Animalsmentioning

confidence: 99%

Mycoplasmas and arthritis.

Hakkarainen¹,

Turunen²,

Miettinen³

et al. 1992

Annals of the Rheumatic Diseases

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The interest in mycoplasmas as human-pathogens has increased again after the discovery of Mycoplasma fermentans strain incognitus in samples from patients with AIDS.`'3 The role of mycoplasmas as causative agents in arthritis has been considered since they were found 50 years ago in rats and mice with arthritis.' Their role in human arthritis remains unsolved, however; several workers have been unable to subcultivate primary mycoplasma isolates in cell free media.

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“…lb). Treatment with 50 mg/kg was chosen since this dosage has been shown to be effective in experimental models of arthritis in both mice [49] and rats [50,51]. The highest concentration of gold was present 1 day following injection (Fig.…”

Section: Gold Concentrations In Plasma Lung and Am Following In Pivmentioning

confidence: 99%

Effect ofin vivo administration of gold sodium thiomalate on rat macrophage function

1982

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It has been shown that gold accumulates in macrophages. In vitro studies have also shown that long-term anti-inflammatory and immuno-regulatory effects on these cells may be responsible for the effectiveness of gold in the treatment of rheumatoid arthritis. However, the relevance of this information to the in vivo circumstance is largely untested. In this study, the effect of gold sodium thiomalate (AuTM) on rat alveolar macrophage (AM) lysosomal enzymes, bacterial killing, and metabolic activities associated with phagocytosis were assessed after in vivo administration. The activities of beta-glucuronidase, acid phosphatase, and lysozyme were inhibited 1 day following a single AuTM injection (50 mg/kg, subcutaneous). However, lysozyme returned to normal, while the activities of beta-glucuronidase and acid phosphatase were elevated from 4 to 12 days thereafter. When AuTM was administered weekly for 8 weeks, the activities of acid phosphatase and beta-glucuronidase were elevated throughout, while lysozyme was largely unaffected. The increased lysosomal enzyme activities were not due to contamination of polymorphonuclear leukocytes. These long-term effects of AuTm on enzyme activity were in marked contrast to its in vitro effect which inhibited the activities of beta-glucuronidase and acid phosphatase. No effect of AuTM administration on the release of beta-glucuronidase upon phagocytosis of opsonized zymosan was observed. At 1 day following a single AuTM injection or 3 days after a second weekly injection, in vivo bactericidal activity of AM toward S. aureus was diminished. This bacterial killing defect was not due to decrease phagocytosis; the in vivo binding and ingestion of bacteria were normal. The defect correlated with imparied metabolic activities associated with phagocytosis, namely a significant decrease in the reduction of nitroblue tetrazolium and the stimulation of the hexose monophosphate shunt. This may be an attractive anti-inflammatory effect in light of the destructive potential of the reactive oxygen species produced by macrophages in an arthritic circumstance.

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Sodium Aurothiomalate, Gold Keratinate, and Various Tetracyclines in Mycoplasma-Induced Arthritis of Rodents

Cited by 14 publications

References 14 publications

Inhibition of mycoplasma-induced lymphocyte activation by sodium aurothiomalate

Inhibition of mycoplasma-induced lymphocyte activation by sodium aurothiomalate

Mycoplasmas and arthritis.

Effect ofin vivo administration of gold sodium thiomalate on rat macrophage function

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