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Phospholipase A2 modulates respiratory burst developed by neutrophils in patients with rheumatoid arthritis

Marinela Bostan1, C Galatiuc, M Hirt

  • 1Center of Immunology, Stefan S. Nicolau Institute of Virology, Bucharest, Romania. immunoce@fx.ro

Journal of Cellular and Molecular Medicine
|May 28, 2003
PubMed

Insights

Phospholipase A(2) (PLA(2)) plays a key role in neutrophil activation and superoxide anion release in rheumatoid arthritis (RA). Inhibiting PLA(2) may be crucial for RA immunotherapy.

Area of Science:

  • Immunology
  • Biochemistry
  • Rheumatology

Background:

  • Neutrophils (PMNs) release arachidonic acid (AA) via phospholipase A(2) (PLA(2)) upon activation.
  • AA is implicated in NADPH-oxidase activation and superoxide anion generation by neutrophils.
  • Elevated PLA(2) levels in rheumatoid arthritis (RA) contribute to synovial inflammation.

Purpose of the Study:

  • To investigate the role of PLA(2) in the respiratory burst of PMNs from RA patients.
  • To determine the effect of different agonists on superoxide anion release in RA PMNs.
  • To assess the impact of exogenous arachidonic acid (AA) on PMN respiratory burst.

Main Methods:

  • Isolation of PMNs from RA patients.
  • Measurement of superoxide anion release using amplified chemiluminescence.
  • Treatment of PMNs with phorbol 12-myristate-13-acetate (PMA), calcium ionophore (A23187), and exogenous AA.
  • Assessment of PLA(2) inhibitors (arachidonyl-trifluorometylketone and BEL).

Main Results:

  • PMA stimulated superoxide anion release in a dose-dependent manner.
  • A23187 did not significantly induce superoxide anion release in RA PMNs.
  • Exogenous AA amplified PMA-induced and, to a lesser extent, A23187-induced superoxide anion release.
  • AA reversed the inhibitory effects of PLA(2) inhibitors.

Conclusions:

  • Different PLA(2) isoforms are likely activated by PMA and A23187, serving distinct functions.
  • PLA(2) activation is critical for the respiratory burst in RA PMNs.
  • PLA(2) inhibition holds potential for RA immunotherapy.

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