There is good scientific evidence that dietary fatty acid composition is involved in the aetiology of many diseases. Increasing the supply of n−3 polyunsaturated fatty acids (PUFA) may reduce the risk of CHD. Several scientific organizations (for example, see Department of Health, 1991, 1994; British Nutrition Foundation, 1992; Scientific Committee for Food, 1993; Food and Agriculture Organization/World Health Organization, 1998) have made recommendations for n−3 PUFA; however, there is a high degree of variation both in terms of the type and amount of n−3 PUFA (up to 7-fold). This variation reflects the different scientific axioms which underlie the different recommendations. Optimal nutrition may be defined in terms of the level of a nutrient required to avoid deficiency, or the amount required to have an effect on biomarkers and functional indicators of nutrient intake, or the level of a nutrient which prevents disease. Functional biomarkers of n−3 PUFA include plasma, platelet and erythrocyte phospholipid-n−3 PUFA levels. Plasma triacylglycerol concentrations represent a functional indicator of n−3 PUFA because n−3 PUFA exert a consistent hypotriacylglycerolaemic effect which is dose-dependent and persistent. In terms of disease status, epidemiological studies have demonstrated that the incidence of CHD is inversely associated with consumption of n−3 PUFA. Despite the health benefits of n−3 PUFA, the mean daily intake falls far short of most of the recommendations. Increasing fish intake is the most obvious way to increase n−3 PUFA intake. However, a large percentage (up to 65) of the population do not eat fish. Thus, there is a need for alternative sources of n−3 PUFA, such as functional foods, whose unique fatty acid composition could fortify staple foods thereby promoting optimal levels of n−3 PUFA intake.

One of the most frequently reported immunomodulatory actions of n−3 PUFA is their ability to diminish in vivo lymphocyte proliferation. The purpose of this study was to determine if n−3 PUFA intake affects the kinetics or magnitude of the antigen-driven expansion of CD8+T-lymphocytes in vivo. In this study we utilized a well-characterized model of T-cell immunity (i.e. infection with the intracellular bacterium, Listeria monocytogenes). Weanling BALB/c mice were fed one of two experimental diets that differed solely in fat source. Our control diet contained lard (180g/kg) and was devoid of long-chain n−3 PUFA. The experimental diet contained 150g/kg menhaden fish oil and 30g/kg corn oil, thus providing approximately 8% of energy from long-chain n−3 PUFA. After 4 weeks, mice were infected intravenously with 106 colony-forming units of actA-deficient L. monocytogenes. Clonal expansion of antigen-specific CD8+T-cells in the spleen was measured at 5, 7, 9 and 14d post-challenge using a class I MHC tetramer loaded with the immunodominant peptide from this pathogen (i.e. Kd:LLO91–99). We report that feeding mice a diet rich in n−3 fatty acids did not significantly impact either the kinetics or magnitude of in vivo, antigen-driven expansion of CD8+T-cells. Furthermore, contraction of this T-cell population was not affected by n−3 PUFA treatment. To our knowledge this is the first time MHC tetramers have been used to investigate the influence of n−3 PUFA on in vivo CD8+T-cell proliferation.