Modulation in vitro of human natural cytotoxicity, lymphocyte proliferative response to mitogensy and cytokine production by essential fatty acids

P. Purasiri*, A. Mckechnie, S. D. Heys, O. Eremin

*Corresponding author for this work

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

Essential fatty acids (EFA) have been shown in animal studies to have a differential effect on various aspects of immune reactivity. However, there have been few studies in humans. Therefore, we elected to investigate the effects of a variety of EFA [gamma-linolenic acid (GLA), eicosapentaenoic acid (EPA) and doeosahexaenoic acid (DHA)] in vitro on human blood lymphocyte reactivity, cytokine secretion and natural cytotoxicity. The proliferative response to polyclonal mitogens (phytohaemagglutinin, pokeweed mitogen, concanavalin A), as measured by [3H]thymidine incorporation into newly synthesized lymphocytes, was inhibited (P<0.05) by all EFAs tested, in a dose-dependent manner (3-15 μg/ml). The greatest inhibition of proliferation was caused by EPA and DHA. Similarly, EPA, DHA and GLA significantly reduced cytotoxic activity [expressed as lyric units, using 51 chromium-release assays, natural killer (NK) (K562 cells) and lymphokine-activated (LAY) (Daudi cells) cells] (P<0.05) in a concentration-dependent manner (5-50 μg/ml), without affecting cell viability. EPA and DHA exhibited greater suppression than GLA. Furthermore, the inhibition of cell proliferation and suppression of natural cytotoxicity was associated with marked decrease in cytokine [interleukin-1 (IL-1), IL-2, tumour necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)] production in vitro. Our findings demonstrate that EFAs (GLA, EPA, DHA) have the potential to inhibit significantly various aspects of human lymphocyte cell-mediated and humoral immune reactivities.

Original languageEnglish
Pages (from-to)166-172
Number of pages7
JournalImmunology
Volume92
Issue number2
DOIs
Publication statusPublished - 30 Oct 2003

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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