Food Lipids: Chemistry, Nutrition, and Biotechnology

guinea pigs showed increased immune function with a doubling of baseline serum
cholesterol but a significant reduction when concentrations of cholesterol were elevated
fourfold. This suggests that there may be species specificity as well as specific
ranges of serum cholesterol levels that modulate immune responses. Most human
studies of lymphocyte function, in vivo or in vitro, have shown decreased functions
in the presence of high total or LDL cholesterol [9]. However, the total number of
circulating T-lymphocyte subsets CD3 � , CD4 � , and CD8 � in hypercholesterolemic
children correlates with LDL cholesterol concentrations over a threefold range [10].
Since T lymphocytes are found in significant numbers in atherosclerotic plaques, it
is presumed that the elevated LDL levels are associated with both development of
arterial lesions and changes seen with chronic inflammation.
Monocyte and macrophage functions are reduced in most studies that have
examined the effect of excess cholesterol. Similarly, functions of the polymorphonuclear
leukocyte have also been reduced in response to a surplus of cholesterol.
The functions are, to a great extent, dependent on plasma membrane microviscosity;
excess cholesterol incorporation will stiffen the membranes, thereby decreasing the
ability of these cells to engulf microbes. A variety of other immune functions have
been examined under the influence of different concentrations of cholesterol, and
most studies show generally reduced immune cell responses; however, there is considerable
disagreement in the research literature on the overall effect of cholesterol
on immune reactions. Reports generally agree that there is reduced resistance to
bacterial or viral infections, but some specific components of the immune system
are suppressed while others are enhanced in the presence of hypercholesterolemia.
With the view that atherosclerosis shares many traits of a chronic inflammatory
condition gaining widespread acceptance only in the late 1980s, the role of cholesterol
in the human immune response as it relates to the development of arterial
lesions has been of considerable interest. Since a large percentage of the fat-filled
foam cells in atheroma are derived from macrophages, it is logical to assume that
cytokines and classical inflammatory repair mechanisms are at work as part of the
atherogenic process.
B. Fatty Acids
Just as cholesterol plays a major role in determining the physical state of the cell
membrane, so do fatty acids. The more polyunsaturated a fatty acid molecule is, the
more fluidity it imparts to the cell membrane. Also, the more polyunsaturated fat in
the diet, the lower the immune response, within certain limits. That is, the immune
response does not go down to zero in the presence of very high intake of polyunsaturated
fat; it is, however, lower relative to that seen with ingestion of saturated
fats. In both humans and animals, cell membrane phospholipids reflect dietary intake
within limits of the membrane to accommodate a certain range of fatty acids. Dietary
fat primarily alters storage of fatty acids in adipose tissue, but smaller changes in
the membranes of many other cell types, including those of the RES, have been
reported. A variety of experimental studies have demonstrated that both the amount
and type of fatty acids consumed have roles to play in altering immune responses.
Although it is easier to discuss specific fatty acids in the diet, it should be remembered
that there are very few free fatty acids consumed and most are in triacylglycerol
molecules, which are usually a mixture of two or three different fatty acids attached
Copyright 2002 by Marcel Dekker, Inc. All Rights Reserved.