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Impaired interleukin-8-dependent chemotaxis by synovial fluid polymorphonuclear leukocytes in rheumatoid arthritis

H Hashimoto1, M Yamamura, K Nishiya

  • 1Third Department of Internal Medicine, Okayama University Medical School, Japan.

Acta Medica Okayama
|August 1, 1994
PubMed

Insights

Polymorphonuclear leukocytes (PMN) in rheumatoid arthritis (RA) synovial fluid show reduced chemotaxis. This impaired cell migration to inflammation sites suggests a defect acquired after entering the joint fluid.

Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Polymorphonuclear leukocytes (PMN) accumulate in synovial fluid during rheumatoid arthritis (RA).
  • The function of these cells within the joint is crucial for understanding RA pathogenesis.

Purpose of the Study:

  • To investigate the chemotactic response of PMN from rheumatoid arthritis patients' synovial fluid compared to peripheral blood.
  • To determine if IL-8 and FMLP induce differential responses in PMN based on their location (synovial fluid vs. peripheral blood).

Main Methods:

  • Utilized a modified Boyden's method to assess PMN chemotaxis.
  • Employed interleukin-8 (IL-8) and N-formyl-methionyl-leucyl-phenylalanine (FMLP) as chemotactic agents.
  • Compared chemotactic responses of synovial fluid PMN and peripheral blood PMN from the same RA patients.

Main Results:

  • Peripheral blood PMN from RA patients showed normal chemotactic response to IL-8 compared to healthy controls.
  • PMN from RA synovial fluid exhibited a significantly decreased chemotactic response to IL-8 and FMLP compared to their peripheral blood counterparts.
  • The reduced chemotactic ability of synovial fluid PMN was inversely correlated with the number of infiltrating cells in the synovial fluid.

Conclusions:

  • PMN chemotactic function is impaired after migration into the synovial fluid of RA patients.
  • This defect may influence the inflammatory process and cell infiltration dynamics in rheumatoid arthritis.
  • Synovial fluid environment may induce functional changes in PMN relevant to RA pathology.

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