Effect of linoleic acid on endothelial cell inflammatory mediators

Valerie M. Young, Michal Toborek, Fajun Yang, Craig J. McClain, Bernhard Hennig

Research output: Contribution to journalArticlepeer-review

72 Scopus citations


Selected lipids may influence the inflammatory cascade within the vascular endothelium. To test this hypothesis, endothelial cells were treated with linoleic acid (18:2, n - 6) for 12 hours and/or tumor necrosis factor- α (TNF) for 4 hours. For a combined exposure to 18:2 and TNF (18:2 + TNF), cells were first preenriched with 18:2 for 8 hours before exposure to TNF for an additional 4 hours. Exposure to 18:2 increased cellular oxidative stress, activated nuclear factor-κB (NF-κB), increased interleukin-8 (IL-8) production, and elevated intercellular adhesion molecule-1 (ICAM-1) levels. A combined exposure to 18:2 + TNF resulted in decreased NF-κB activation compared with TNF treatment alone. In addition, preexposure to 18:2 altered TNF-mediated IκB-α signaling. Within the first 15 minutes of a 90-minute period, cytoplasmic levels of IκB-α decreased more rapidly in cells treated with 18:2+TNF compared with TNF, suggesting translocation and activation of NF-κB in cultures that were pretreated with 18:2 before TNF exposure. A combined exposure to 18:2+TNF had various effects on IL-8 production and ICAM-1 levels depending on the time of exposure. For example, 18:2+TNF treatment increased ICAM-1 levels at 12 hours but decreased ICAM-1 levels at 24 hours compared with treatment with TNF alone. These data suggest that selected fatty acids such as 18:2 can exert proinflammatory effects and, in addition, may markedly alter TNF-mediated inflammatory events.

Original languageEnglish
Pages (from-to)566-572
Number of pages7
JournalMetabolism: Clinical and Experimental
Issue number5
StatePublished - 1998

Bibliographical note

Funding Information:
From the Departments of Nutrition and Food Science, Surgery, and Medicine, University of Kentucky, Lexington, KY. Submitted May 30, 1997; accepted November 10, 1997. Supported in part by grants from the National Institutes of Health, American Heart Association Kentucky Affiliate, US Department of Agriculture, University of Kentucky Research Funds, an American Cancer Society Institutional Research Grant, and the Kentucky Agricultural Experiment Station. Address reprint requests to Bernhard Hennig, PhD, Cell Nutrition Group, Department of Nutrition and Food Science, 204 Funkhouser Building, University of Kentucky, Lexington, KY40506-0054. Copyright © 1998 by W,B. Saunders Company 0026-0495/98/4705-0013503.00/0

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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