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 | |
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Abstract | 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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AbstractList | 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. |
Author | ZURIER, Robert B SEILER, Christina M FURSE, Robert K ROSSETTI, Ronald G |
Author_xml | – sequence: 1 givenname: Robert K surname: FURSE fullname: FURSE, Robert K organization: University of Massachusetts Medical School, Department of Medicine, 55 Lake Avenue North, Worcester, Massachusetts 01655, United States – sequence: 2 givenname: Ronald G surname: ROSSETTI fullname: ROSSETTI, Ronald G organization: University of Massachusetts Medical School, Department of Medicine, 55 Lake Avenue North, Worcester, Massachusetts 01655, United States – sequence: 3 givenname: Christina M surname: SEILER fullname: SEILER, Christina M organization: University of Massachusetts Medical School, Department of Medicine, 55 Lake Avenue North, Worcester, Massachusetts 01655, United States – sequence: 4 givenname: Robert B surname: ZURIER fullname: ZURIER, Robert B organization: University of Massachusetts Medical School, Department of Medicine, 55 Lake Avenue North, Worcester, Massachusetts 01655, United States |
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Keywords | Human Monocyte Immunomodulation Interleukin 1 receptor antagonist Cytokine Interleukin 1 Oral administration Unsaturated fatty acid Inflammation Biological activity γ-Linolenic acid |
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Title | Oral administration of gammalinolenic acid, an unsaturated fatty acid with anti-inflammatory properties, modulates interleukin-1β production by human monocytes |
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