Oral administration of gammalinolenic acid, an unsaturated fatty acid with anti-inflammatory properties, modulates interleukin-1β production by human monocytes

• Published in: Journal of clinical immunology Vol. 22; no. 2; pp. 83 - 91
• Main Authors: FURSE, Robert K, ROSSETTI, Ronald G, SEILER, Christina M, ZURIER, Robert B
• Format: Journal Article
• Language: English
• Published: New York, NY Kluwer/Plenum 01.03.2002
• Subjects: Biological and medical sciences; fatty acids; g-linolenic acid; Immunomodulators; interleukin 1^b; Medical sciences; Pharmacology. Drug treatments; Human; Monocyte; Immunomodulation; Interleukin 1 receptor antagonist; Cytokine; Interleukin 1; Oral administration; Unsaturated fatty acid; Inflammation; Biological activity; γ-Linolenic acid
• DOI: 10.1023/A:1014479702575
• ISSN: 0271-9142

Administration of gammalinolenic acid (GLA), an unsaturated fatty acid, reduces joint inflammation in patients with rheumatoid arthritis. Addition of GLA in vitro suppresses release of interleukin-1 beta (IL-1 beta ) from human monocytes stimulated with lipopolysaccharide (LPS). LPS-induced IL-1 beta release is followed by IL-1-induced IL-1 beta release, an amplification process termed "autoinduction." We show here, using IL-1 alpha stimulation to simulate autoinduction, that administration of GLA to healthy volunteers and to patients with inflammatory arthritis reduces LPS-induced IL-1 beta secretion mainly by reducing autoinduction of IL-1 beta . GLA reduces LPS-induced pro-IL-1 beta mRNA modestly and IL-1 alpha -induced pro-IL-1 beta gene expression markedly. In addition to reducing amplification of IL-1 beta , GLA increases the amount of IL-1 receptor antagonist (IL-1Ra) secreted from stimulated cells, thereby facilitating an increase in the secreted IL-1Ra/IL-1 beta ratio. IL-1 beta is important to host defense, but the amplification mechanism may be excessive in genetically predisposed individuals. Thus, reduction of IL-1 beta autoinduction may be protective in some patients with endotoxic shock and with diseases characterized by chronic inflammation.