Food Lipids: Chemistry, Nutrition, and Biotechnology

phocytes, increases proliferation of cytotoxic T cells, and enhances rejection of skin
grafts in mice [5]. Similar data from humans were also seen: a low-carotenoid diet
led to decreased delayed-type skin hypersensitivity reactions (mediated by T cells),
and supplementation with �-carotene restored the skin reactions to normal [6].
Although a variety of cell-based mechanisms that do not involve eicosanoids
have been proposed for modulating the immune response, perhaps some of the
strongest evidence comes from studies of general nutritional status. Both overnutrition
and energy restriction have profound effects on the immune system’s regulation.
Overnutrition that results in obesity depresses the immune response, while energy
restriction that avoids nutrient deficiencies enhances the immune response, particularly
in older animals [7].
III. DIETARY LIPIDS
A. Cholesterol
Dietary cholesterol has been studied extensively for its effects on immune functions,
primarily in animals and in vitro. A fair number of studies in humans have been
conducted, however. The rationale for this work is that cholesterol and fatty acids
in the cell membrane are the primary determinants of membrane microviscosity,
which in turn controls a number of events at the cell surface, including enzymatic
activities such as those of phospholipase and cyclooxygenase. There is considerable
variation in serum cholesterol concentrations among humans, but two factors have
contributed to the relatively small number of studies showing a positive correlation
between dietary cholesterol and changes in the immune response. First, dietary cholesterol
is relatively weak in its ability to increase serum cholesterol. Second, the
populations studied have not exhibited a broad enough range of serum cholesterol
concentrations to permit observation of large effects on immunological functions in
vivo (although some studies have noted differential responses in vitro). Therefore,
experimental manipulations in animals or in vitro that entailed extreme differences
in exposure to cholesterol have resulted in significant effects on immunologic
responses.
It is impossible to singularly characterize the effect of cholesterol on immunologic
responses. This is because cholesterol is delivered to cells in lipoproteins,
complex aggregates of cholesterol, triglyceride, phospholipid, and one or more apoproteins
to a variety of immunologic cells. It has been shown that isolated apolipoprotein
E (apoE) inhibits lymphocyte proliferation, but its effectiveness depends on
interaction with cholesterol and phospholipid. Recent interest in the role of oxidized
lipoproteins in the development of atherosclerosis suggests that some of the immunologic
effects attributed to cholesterol may have been due to oxidized cholesterol
molecules. In fact, there is considerable evidence that oxidized low density lipoprotein
(LDL) or cholesterol reduces immune responses by lymphocytes.
The change in immunologic response elicited by elevated cholesterol concentrations
depends both on the concentration of cholesterol to which cells are exposed
and the type of immunologic response being measured. There is no single direction.
Most studies in this area have looked at lymphocyte functions, and it can be concluded
that results are primarily dependent on lipoprotein concentration [8].
Studies done in hypercholesterolemic rabbits and monkeys suggest that both
B- and T-cell-dependent functions are elevated. However, hypercholesterolemic
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