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Activated monocytes induce arthritis-associated changes in mitochondria of cultured synovial fibroblasts

K J Pulkki1, E T Eerola, R M Saario

  • 1Department of Medical Biochemistry, University of Turku, Finland.

Scandinavian Journal of Rheumatology
|January 1, 1988
PubMed

Insights

Monocytes in inflammatory arthritis can alter normal fibroblasts, causing increased autofluorescence and abnormal mitochondria. This reveals a new interaction in synovial inflammation.

Area of Science:

  • Cell Biology
  • Immunology
  • Rheumatology

Background:

  • Synovial fibroblasts from arthritis patients show increased autofluorescence and mitochondrial anomalies.
  • These changes are linked to inflammatory synovial tissue in rheumatoid and non-rheumatoid arthritis.

Purpose of the Study:

  • To investigate the cause of increased autofluorescence and mitochondrial abnormalities in synovial fibroblasts.
  • To explore the role of mononuclear cells in inducing these changes in normal fibroblasts.

Main Methods:

  • Normal synovial fibroblasts were exposed to conditioned media from stimulated monocytes.
  • Changes in autofluorescence and mitochondrial morphology were analyzed.
  • The effects of indomethacin, gold salts, and cycloheximide were assessed.

Main Results:

  • Conditioned media from lipopolysaccharide- or poly-IC-stimulated monocytes induced autofluorescence and mitochondrial changes in normal fibroblasts.
  • These induced changes mimicked those observed in fibroblasts from arthritis patients.
  • Indomethacin and gold salts did not prevent these effects, but cycloheximide did.

Conclusions:

  • Monocyte-derived factors can induce cellular changes in synovial fibroblasts characteristic of arthritis.
  • This highlights a novel monocyte-fibroblast interaction in synovial inflammation.
  • These findings offer new insights into the pathogenesis of inflammatory arthritis.

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