Feeding rats or mice diets deficient in n-6 or n-3 fatty acids decreased neu-trophil chemotaxis and macrophage-mediated phagocytic and cytotoxic activity, as compared with animals fed diets containing adequate amounts of these fatty acids (for references, see Kelley and Daudu, 1993). Thus, the immunolog-ical effects of essential fatty-acid deficiencies on innate immune responses are similar to the effects of other essential nutrient deficiencies. However, again as seen with other essential nutrients, an excess of essential fatty acids can impair aspects of the innate immune response. Animal studies have reported lower natural killer cell activity following the feeding of high fat including oils rich in linoleic acid (maize, sunflower or safflower oil) or in a-linolenic acid (e.g. linseed (flaxseed) oil), when compared with feeding high-saturated-fat diets (for references, see Kelley and Daudu, 1993; Calder, 1998a, b). These data suggest that a very high intake of linoleic or a-linolenic acid, compared with saturated fatty acids, has the potential to suppress natural killer cell activity. However, in humans, increasing linoleic acid intake by 6 g day-1 did not affect natural killer cell activity or the production of cytokines (interleukin (IL)-1p, tumour necrosis factor (TNF)-a) by monocytes (Yaqoob et al., 2000). Furthermore, increasing a-linolenic acid intake by 2 or 4 g day-1 (less than usually fed in animal studies) did not affect natural killer cell activity or the production of TNF-a, IL-1p or IL-6 by monocytes (Thies et al., 2001a, b), neutrophil respiratory burst (Healy et al., 2000; Thies et al., 2001b) or monocyte respiratory burst (Thies et al., 2001b). This suggests that the amount of essential fatty acids that humans could potentially consume in the habitual diet is not sufficient to negatively influence innate immunity. However, feeding a high dose of a-linolenic acid (approx. 15 g day-1) was reported to decrease IL-1 and TNF production by human monocytes (Caughey et al., 1996).
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