Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Br J Nutr. 2004 Jun;91(6):893-903.

The influence of different combinations of gamma-linolenic acid, stearidonic acid and EPA on immune function in healthy young male subjects.

Author information

  • 1Institute of Human Nutrition, School of Medicine, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK. eam@soton.ac.uk

Abstract

To determine the effects of EPA, stearidonic acid (STA) or gamma-linolenic acid (GLA) on immune outcomes, healthy male subjects consumed one of seven oil blends for 12 weeks. EPA consumption increased the EPA content of peripheral blood mononuclear cells (PBMC). Consumption of GLA (2.0 g/d) in the absence of STA or EPA increased di-homo-GLA content in PBMC. Neither STA nor its derivative 20 : 4n-3 appeared in PBMC when STA (<1.0 g/d) was consumed. However, STA (1.0 g/d), in combination with GLA (0.9 g/d), increased the proportion of EPA in PBMC. None of the treatments altered neutrophil or monocyte phagocytosis or respiratory burst, production of inflammatory cytokines by monocytes, T lymphocyte proliferation or the delayed-type hypersensitivity response. Production of cytokines by T lymphocytes increased in all groups, with no differences among them. The proportion of lymphocytes that were natural killer cells decreased significantly in subjects receiving 2.0 g EPA or GLA/d. There were no other effects on lymphocyte sub-populations. Plasma IgE concentration decreased in most groups, but not in the control group. Plasma IgG2 concentration increased in the EPA group. Thus, EPA or GLA at a dose of 2.0 g/d have little effect on key functions of neutrophils, monocytes and T lymphocytes, although at this dose these fatty acids decrease the number of natural killer cells. At this dose EPA increases IgG2 concentrations. STA can increase immune cell EPA status, but at 1.0 g/d does not affect human immune function.

PMID:
15182393
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Cambridge University Press
    Loading ...
    Write to the Help Desk