Phospholipase A2, prostaglandin E2 and polyunsaturated fatty acid metabolic abnormalities in multiple sclerosis

Authors

  • Gloudina M. Hon,

    Corresponding author
    1. Department of Bio-Medical Sciences, Faculty of Health and Wellness Science, Cape Peninsula University of Technology, Bellville, Cape Town, South Africa
    • Correspondence

      Gloudina Hon, DTech, Biomedical Technology, Faculty of Health and Wellness Science, Cape Peninsula University of Technology, PO Box 1906, Bellville, 7530,

      Cape Town, South Africa.

      Tel: +27-21-959-6015

      Fax: +27-21-959-6760

      Email: hong@cput.ac.za

    Search for more papers by this author
  • Rajiv T. Erasmus,

    1. Division of Chemical Pathology, University of Stellenbosch, Tygerberg Campus, Tygerberg, South Africa
    Search for more papers by this author
  • Tandi E. Matsha

    1. Department of Bio-Medical Sciences, Faculty of Health and Wellness Science, Cape Peninsula University of Technology, Bellville, Cape Town, South Africa
    Search for more papers by this author

Abstract

Aim

Metabolic abnormalities reported in patients with multiple sclerosis include a decrease in cell membrane fatty acid C20:4n-6. The aim of the present study was to investigate whether this decrease was associated with abnormalities in the prostaglandin E2 pathway in patients with multiple sclerosis.

Methods

The study population included 31 patients with multiple sclerosis and 30 healthy controls. Peripheral blood mononuclear cell membrane fatty acids were measured by gas chromatography, secretory-phospholipase A2, and prostaglandin E2 with enzyme-linked immunosorbent assays and C-reactive protein with a Beckman auto-analyser.

Results

Prostaglandin E2 was increased in patients (545.5 pg/mL; quartile range 585.1 pg/mL) and controls (248.2 pg/mL; quartile range 183.6 pg/mL; P = 0.0018). Phospholipase A2 was inversely associated with C20:4n-6 in patients and controls, respectively (P = 0.0398 and P = 0.0182). C-reactive protein showed a positive association with phospholipase A2 in patients (P = 0.0006), and an inverse association with prostaglandin E2 in controls (P = 0.0006).

Conclusions

The increase in prostaglandin E2 concentration in plasma from patients with multiple sclerosis was possibly enhanced by the positive association between the C-reactive protein and phospholipase A2 concentrations present in patients; that is, active stimulation of the prostaglandin E2 pathway, which can possibly explain decreases in membrane n-6 fatty acid C20:4n-6 reported in cell membranes from patients. It is not clear from the results of the present study whether this denotes chronic inflammation in patients, but could be expected to contribute to central nervous system damage reported in patients with multiple sclerosis.

Ancillary