Gammalinolenic acid, an unsaturated fatty acid with anti-inflammatory properties, blocks amplification of IL-1 beta production by human monocytes
Department of Medicine, Division of Rheumatology
Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Cell Separation; Cells, Cultured; Dose-Response Relationship, Drug; Dose-Response Relationship, Immunologic; Female; Gene Expression Regulation; Humans; Interleukin-1; Lipopolysaccharides; Macrophage Activation; Middle Aged; Monocytes; Protein Precursors; RNA, Messenger; gamma-Linolenic Acid
Life Sciences | Medicine and Health Sciences
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 IL-1beta from human monocytes stimulated with LPS. LPS-induced IL-1beta release is followed by IL-1-induced IL-1beta release, an amplification process termed autoinduction. We show here with peripheral blood monocytes from normal volunteers and from patients with rheumatoid arthritis by using IL-1R antagonist to block autoinduction and IL-1alpha stimulation to simulate autoinduction that approximately 40% of IL-1beta released from LPS-stimulated cells is attributable to autoinduction and that GLA reduces autoinduction of IL-1beta while leaving the initial IL-1beta response to LPS intact. Experiments with cells in which transcription and protein synthesis were blocked suggest that GLA induces a protein that reduces pro-IL-1beta mRNA stability. IL-1beta is important to host defense, but the amplification mechanism may be excessive in genetically predisposed patients. Thus, reduction of IL-1beta autoinduction may be protective in some patients with endotoxic shock and with diseases characterized by chronic inflammation.
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Citation: J Immunol. 2001 Jul 1;167(1):490-6.
Journal of immunology (Baltimore, Md. : 1950)
Furse, Robert K.; Rossetti, Ronald G.; and Zurier, Robert, "Gammalinolenic acid, an unsaturated fatty acid with anti-inflammatory properties, blocks amplification of IL-1 beta production by human monocytes" (2001). Open Access Articles. 1126.