Cyclosporin A prevents the histologic damage of antigen arthritis without inducing fibrosis

M J Benito1, O Sánchez-Pernaute, M J López-Armada

  • 1Fundación Jiménez Díaz, and Universidad Autónoma, Madrid, Spain.

Arthritis and Rheumatism
|February 29, 2000
PubMed
Abstract

Insights

Cyclosporin A (CSA) prevents chronic synovitis in rheumatoid arthritis (RA) models by reducing tissue damage and normalizing growth factor expression. However, CSA also increases growth factor gene expression in healthy synovial cells in vitro.

Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Rheumatoid arthritis (RA) involves chronic synovitis and pannus development.
  • Growth factors like TGF-beta and PDGF-B are implicated in RA pathogenesis.
  • Cyclosporin A (CSA) is an immunosuppressant with potential anti-inflammatory effects.

Purpose of the Study:

  • To investigate the effects of CSA on a rabbit model of RA.
  • To assess CSA's impact on growth factor activation and pannus development.
  • To examine CSA's influence on synovial cell gene expression.

Main Methods:

  • Induced antigen arthritis in rabbit knees, treated with CSA or solvent.
  • Analyzed synovial tissues for histopathology, collagen, TGF-beta, and PDGF-B mRNA.
  • Examined CSA's effect on TGF-beta and PDGF-B expression in cultured synovial cells.

Main Results:

  • CSA treatment reduced histologic damage and matrix deposition in vivo.
  • CSA normalized elevated TGF-beta and PDGF-B expression in treated rabbits.
  • CSA dose-dependently upregulated TGF-beta and PDGF-B gene expression in healthy cultured synovial cells.

Conclusions:

  • Continuous CSA administration prevents chronic synovitis in experimental RA.
  • CSA modulates growth factor expression in vivo but upregulates it in vitro.
  • CSA's profibrogenic effect was not observed in the inflamed RA environment.

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