There are many published animal studies investigating the effects of fish oil on aspects of inflammation and innate immunity. Most of these studies indicate that feeding high amounts of fish oil decreases a wide range of responses. However, not all studies agree with this generalization. Animal studies are often designed to demonstrate effects and to identify potential mechanisms and so result in the use of diets that differ markedly from human diets in both the level and the type of fat. Additional reasons for apparent contradictions in this literature might relate to the species of animal studied, the comparison being made (e.g. to a low-fat diet or to another high-fat diet; to saturated fat or to a diet high in n-6 PUFAs), the amount of vitamin E in the diets and the conditions used for ex vivo cell-culture experiments.
Feeding fish oil to laboratory animals has been reported to decrease macrophage functions, including generation of reactive oxygen species and production of TNF-a, IL-1 and IL-6 (e.g. Billiar et al., 1988; Hubbard et al., 1991; Renier et al., 1993). Fish oil, compared with other fat sources, resulted in lower concentrations of TNF-a, IL-1 p and IL-6 in the bloodstream after endotoxin injection or burns (e.g. Hayashi et al., 1998; Sadeghi et al., 1999). Thus, these studies support the idea that fish oil has anti-inflammatory effects. There are, however, opposing studies. For example, Somers et al. (1989) reported that cultured peritoneal macrophages from mice fed fish-oil-supplemented diets exhibited higher TNF-a activity after endotoxin stimulation than did macrophages from mice fed a diet high in linoleic acid.
Animal feeding studies indicate that feeding high levels of fish oil decreases natural killer cell activity (e.g. Meydani et al., 1988; Yaqoob et al., 1994a), while lower levels (e.g. EPA plus DHA fed at less than 5% w/w of the diet) are reported to enhance this activity (Brouard and Pascaud, 1993; Robinson and Field, 1998). This effect may also be fatty-acid-specific, as a recent study reported that relatively low levels (4.4% of fatty acids; 1.7% of energy) of dietary EPA (but not DHA) inhibit rat natural killer cell activity (Peterson et al., 1998).
Human studies have generally fed proportionately less fish oil than the amount provided in most animal studies. Nevertheless, a number of studies in healthy humans reveal significant immunomodulatory effects of long-chain n-3 PUFAs. Providing more than 2.3 g EPA plus DHA day-1 (and in some studies up to 14.5 g day-1) has been reported to decrease chemotaxis and superoxide production by neutrophils (Lee et al., 1985; Schmidt et al., 1989, 1992; Luostarinen et al., 1992; Sperling et al., 1993) and by monocytes (Endres et al., 1989; Schmidt et al., 1989, 1992; Fisher et al., 1990). Daily consumption of more than 2.4 g EPA plus DHA day-1 has been shown in some studies to decrease production of TNF, IL-1 and IL-6 by mononuclear cells (Endres et al., 1989; Meydani et al., 1991; Gallai et al., 1993; Caughey et al., 1996). Similarly, adding oily fish (providing 1.2 g EPA plus DHA day-1) to a low-fat diet resulted in decreased production of TNF, IL-1 and IL-6 (Meydani et al., 1993). Parenteral nutrition supplemented with fish oil decreased serum TNF-a and IL-6 concentrations in patients following major abdominal surgery, compared with n-6 fatty-acid-rich parenteral nutrition (Wachtler et al., 1997). In contrast to these observations, a number of studies that provided from 0.55 g to 3.4 g EPA plus DHA day-1 failed to demonstrate an effect on neutrophil chemotaxis, neutrophil or monocyte respiratory burst or the production of TNF, IL-1 and IL-6 (Molvig et al., 1991; Cooper et al., 1993; Schmidt et al., 1996; Blok et al., 1997; Healy et al., 2000; Yaqoob et al., 2000; Thies et al., 2001b).
Thus, studies in animals and humans have demonstrated that high levels of fish oil or its component n-3 PUFAs in the diet exert potent anti-inflammatory effects, particularly decreasing neutrophil and monocyte chemotaxis, superoxide production and production of pro-inflammatory cytokines. Reduced production of pro-inflammatory mediators may be beneficial in diseases characterized by excess production of these mediators (see later sections). On the other hand, these effects may compromise immune function in healthy and immune-compromised individuals. The effects of these lipids are probably dose-dependent (and disease-specific), as studies providing more modest amounts of long-chain n-3 PUFAs have not consistently demonstrated these effects on the innate immune system.
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