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Proinflammatory cytokines enhance human synoviocyte expression of functional intercellular adhesion molecule-1

H B Lindsley1, D D Smith, C B Cohick

  • 1Department of Medicine, University of Kansas Medical Center, Kansas City 66160.

Clinical Immunology and Immunopathology
|September 1, 1993
PubMed

Insights

Proinflammatory cytokines like IL-1 beta and TNF alpha significantly increase ICAM-1 expression on human synoviocytes, enhancing the adhesion of peripheral blood mononuclear cells (PBMCs). This finding is relevant for understanding inflammatory cell interactions in joints.

Area of Science:

  • Immunology
  • Cell Biology
  • Rheumatology

Background:

  • Synoviocytes play a crucial role in joint inflammation.
  • Intercellular Adhesion Molecule-1 (ICAM-1) is involved in immune cell trafficking.
  • The role of cytokines in modulating synoviocyte function requires further elucidation.

Purpose of the Study:

  • To investigate the effect of proinflammatory cytokines on ICAM-1 expression in human synoviocytes.
  • To determine the impact of these cytokines on peripheral blood mononuclear cell (PBMC) adhesion to synoviocytes.
  • To compare responses in synoviocytes from patients with rheumatoid arthritis and osteoarthritis.

Main Methods:

  • Cell ELISA and flow cytometry were used to characterize surface molecule expression.
  • PBMC adhesion assays were performed using direct counting and colorimetric staining.
  • Kinetic and concentration-dependent studies were conducted for various cytokines.

Main Results:

  • IL-1 beta, TNF alpha, and IFN-gamma significantly upregulated ICAM-1 expression on synoviocytes.
  • PBMC adhesion to synoviocytes was increased by IL-1 beta and TNF alpha.
  • Cytokine-induced ICAM-1 upregulation and PBMC adhesion were observed in both rheumatoid and osteoarthritis synoviocytes.

Conclusions:

  • Proinflammatory cytokines enhance ICAM-1 expression and PBMC adhesion on human synoviocytes.
  • This cytokine-mediated increase in synoviocyte adhesiveness may facilitate inflammatory cell infiltration into joints.
  • Findings provide insights into the cellular mechanisms underlying joint inflammation in rheumatic diseases.

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