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Phospholipase A 2, prostaglandin E 2 and polyunsaturated fatty acid metabolic abnormalities in multiple sclerosis
Author(s) -
Hon Gloudina M.,
Erasmus Rajiv T.,
Matsha Tandi E.
Publication year - 2013
Publication title -
clinical and experimental neuroimmunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.297
H-Index - 15
ISSN - 1759-1961
DOI - 10.1111/cen3.12066
Subject(s) - arachidonic acid , prostaglandin , endocrinology , medicine , fatty acid , phospholipase a2 , polyunsaturated fatty acid , prostaglandin e2 , population , phospholipase , chemistry , biology , biochemistry , enzyme , environmental health
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 A 2, and prostaglandin E 2 with enzyme‐linked immunosorbent assays and C ‐reactive protein with a B eckman auto‐analyser. Results Prostaglandin E 2 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 A 2 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 A 2 in patients ( P  = 0.0006), and an inverse association with prostaglandin E 2 in controls ( P  = 0.0006). Conclusions The increase in prostaglandin E 2 concentration in plasma from patients with multiple sclerosis was possibly enhanced by the positive association between the C ‐reactive protein and phospholipase A 2 concentrations present in patients; that is, active stimulation of the prostaglandin E 2 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.

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