Decreased arachidonic acid release in peripheral blood monocytes of patients with systemic lupus erythematosus

OBJECTIVE: To investigate the release of arachidonic acid (AA) in unfractionated peripheral blood mononuclear cells (PBMC), separated monocytes and T lymphocytes of patients with systemic lupus erythematosus (SLE). METHODS: AA release was measured in cells from 56 patients with SLE and from 48 contr...

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Bibliographic Details
Published in:Journal of rheumatology 2001-09, Vol.28 (9), p.2012-2017
Main Authors: SIPKA, Sandor, SZANTO, Sandor, SZEGEDI, Gyula, SZÜCS, Kornélia, KOVACS, Ildiko, KISS, Emese, ANTAL-SZALMAS, Peter, LAKOS, Gabriella, ALEKSZA, Magdolna, ILLES, Arpad, GERGELY, Pal
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Arachidonic Acid - analysis
Arachidonic Acid - biosynthesis
Biological and medical sciences
Biomarkers - blood
Cells, Cultured
Female
Glucocorticoids - administration & dosage
Humans
Lupus Erythematosus, Systemic - blood
Lupus Erythematosus, Systemic - drug therapy
Male
Medical sciences
Middle Aged
Monocytes - metabolism
Prognosis
Reference Values
Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
Sensitivity and Specificity
Severity of Illness Index
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Summary:OBJECTIVE: To investigate the release of arachidonic acid (AA) in unfractionated peripheral blood mononuclear cells (PBMC), separated monocytes and T lymphocytes of patients with systemic lupus erythematosus (SLE). METHODS: AA release was measured in cells from 56 patients with SLE and from 48 controls. Of the 56 patients with SLE, 38 were receiving glucocorticosteroids and 18 were not. [3H]AA was incorporated into the membranes of PBMC and purified subsets of monocytes and T lymphocytes. The release of [3H]AA was measured both in nonstimulated cells cultured for 24 h and in cell cultures stimulated by phorbol ester (PMA) and Ca2+ ionophore for 4 h. RESULTS: In the PBMC of SLE patients not taking glucocorticosteroids, the release of AA was decreased in both stimulated and nonstimulated cells. There was a decrease of AA production in monocytes but not in T lymphocytes. This phenomenon could be observed in the active and inactive phases of the disease. CONCLUSION: A defect in AA production may exist in the peripheral monocytes of patients with SLE, resulting in decreased release of AA in patients not receiving glucocorticosteroid therapy.
ISSN:0315-162X
1499-2752