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Soluble E-selectin in arthritis

A E Koch1, W Turkiewicz, L A Harlow

  • 1Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611.

Clinical Immunology and Immunopathology
|October 1, 1993
PubMed
Summary
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Soluble E-selectin (sE-selectin) is elevated in the synovial fluid of rheumatoid arthritis patients compared to osteoarthritis patients. This molecule, produced by endothelial cells, may play a role in inflammatory cell migration in rheumatoid arthritis.

Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Cellular adhesion molecules like E-selectin are crucial for recruiting leukocytes to inflammatory sites.
  • A soluble form, soluble E-selectin (sE-selectin), has been identified.
  • Understanding sE-selectin's role in inflammatory joint diseases is important.

Purpose of the Study:

  • To measure sE-selectin levels in synovial fluid (SF) and blood of rheumatoid arthritis (RA) patients.
  • To correlate sE-selectin levels with clinical parameters of disease activity.
  • To investigate the cellular source of sE-selectin in RA.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to quantify sE-selectin in SF, blood, and cell culture supernatants.
  • Samples were obtained from 76 patients with RA and other inflammatory disorders, as well as osteoarthritis (OA) patients.

Related Experiment Videos

  • Human umbilical vein endothelial cells (HUVECs) and RA synovial tissue (ST) cells were cultured.
  • Main Results:

    • SF sE-selectin levels were significantly higher in RA patients compared to OA patients (P < 0.05).
    • SF sE-selectin levels correlated positively with SF leukocyte counts.
    • Endothelial cells from HUVECs and RA STs were found to produce sE-selectin, while RA SF neutrophils did not.

    Conclusions:

    • sE-selectin levels are elevated in the SF of RA patients, suggesting its involvement in the disease.
    • Endothelial cells are a source of sE-selectin in the RA joint.
    • sE-selectin may contribute to the migration of inflammatory leukocytes into RA synovial tissues and fluids.