Oral administration of gammalinolenic acid, an unsaturated fatty acid with anti-inflammatory properties, modulates interleukin-1β production by human monocytes
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 bet...
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Published in | Journal of clinical immunology Vol. 22; no. 2; pp. 83 - 91 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Kluwer/Plenum
01.03.2002
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 0271-9142 1573-2592 |
DOI: | 10.1023/A:1014479702575 |