The development, maintenance, and optimal functioning of the immune system are dependent on balanced and adequate nutrition. However, either a deficiency or an excess of a number of nutrients can have adverse effects. The nutrients with the most pronounced effects in humans include amount and type of dietary fatty acids (FAs), protein energy malnutrition, vitamins A, B6, B12, C, and E, and minerals including zinc, copper, selenium, and iron. Multiple rather than single nutrient deficiencies are often the cause for a compromised immune system. A number of excellent review articles and books deal with the nutritional regulation of immune functions (Amati et al., 2003; Calder and Kew, 2002; Field et al., 2002). Dietary fat can have diverse effects on human health based on the amounts consumed and, more importantly, on the types consumed. Dietary fat may also differentially affect certain cells, tissues, and organs depending on their stage of development. The FA composition of human tissues and organs can vary depending on the types of FAs that are consumed in the diet; that composition has been used as a biomarker for correlation with immunity and risk with disease. In addition, some dietary FAs can be transformed into potent biological mediators that have been shown to initiate or alter numerous processes in the body. For example, linoleic acid (LA, 18:2, n-6), a common component of some vegetable oils, can be converted by a number of cell types into arachidonic acid (AA, 20:4, n-6), a major precursor for the potent immunomodulatory agents, prostaglandin (PG)E 2 and leukotriene (LT)B 4, which are produced from AA by the enzymes cyclooxygenase and 5-lipoxygenase, respectively. Other 20-carbon FAs, eicosapentaenoic acid (EPA, 20:5 n-3), and dihomo-gamma linolenic (DGLA, 20:3, n-6) compete with AA as substrates for these enzymes and, thus, can decrease the production of PGE 2 and LTB 4. The eicosanoids produced from EPA and DGLA consequently have only weak effects on cells of the immune system. Docosahexaenoic acid (DHA, 22:6, n-3) is not a substrate for the cyclooxygenase and lipoxygenase; however, it can inhibit the synthesis of the n-6 eicosanoids by inhibiting the release of membrane AA (Martin, 1998). It can also be retroconverted to EPA. Because PGE 2 and LTB 4 have been linked to alterations in the immune system and to specific pathological processes, dietary fat intake has the potential to alter human disease. Reduced production of inflammatory eicosanoids by DHA, EPA, and DGLA, therefore, forms the basis for their use in the management of inflammatory diseases. In this chapter, we provide a brief introduction to immune system and FA nomenclature. The effects of dietary FAs on the number and activity of the cells of the immune system is a main focal point. We emphasize the results of human studies and discuss animal studies as a means to understand some of the proposed mechanisms by which FAs alter immune functions. The amount of published information for various topics can be quite different, and thus, the amount of detail given varies. Further details can be found in individual papers cited or other reviews regarding the effect of dietary FAs on immune functions (Calder and Grimble, 2002; De Pablo and De Cienfuegos, 2000; Harbige, 2003; Yaqoob and Calder, 2003).
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health
- Nutrition and Dietetics
- Food Science