Effect Of Dietary Lipid Manipulation Research Articles

Immune cell functions, lipids and host natural resistance.

Nutritional status may exert a profound effect on immune system functions. Hence, several parameters of immune system are modified by dietary lipid administration, as lymphocyte proliferation, cytokine production, natural killer activity, antigen presentation, etc. Thus, numerous studies have indicated the key role of lipids as immune response modulators. These properties have been applied in the treatment of autoimmune and inflammatory diseases. As a result, the reduction or suppression of immune status due to lipid incorporation promotes an impairment in the ability of host natural response to eliminate infectious microorganisms as bacteria or parasites. In the present review, we analyze the current status about the relationship among dietary lipids, reduction of immune parameters and reduction of host natural response against infectious diseases. Many discrepancies are discussed, although several studies indicate a close association between dietary lipid manipulation and impairment in the elimination of bacteria, viruses or parasites. On the other hand, other studies point out a beneficial effect of dietary lipid manipulation on the host natural response. Future investigations will determine the events involved in the regulation of immune response by fatty acids and their role in the elimination of pathogenic agents.

Immune cell functions, lipids and host natural resistance

Nutritional status may exert a profound effect on immune system functions. Hence, several parameters of immune system are modified by dietary lipid administration, as lymphocyte proliferation, cytokine production, natural killer activity, antigen presentation, etc. Thus, numerous studies have indicated the key role of lipids as immune response modulators. These properties have been applied in the treatment of autoimmune and inflammatory diseases. As a result, the reduction or suppression of immune status due to lipid incorporation promotes an impairment in the ability of host natural response to eliminate infectious microorganisms as bacteria or parasites. In the present review, we analyze the current status about the relationship among dietary lipids, reduction of immune parameters and reduction of host natural response against infectious diseases. Many discrepancies are discussed, although several studies indicate a close association between dietary lipid manipulation and impairment in the elimination of bacteria, viruses or parasites. On the other hand, other studies point out a beneficial effect of dietary lipid manipulation on the host natural response. Future investigations will determine the events involved in the regulation of immune response by fatty acids and their role in the elimination of pathogenic agents.

Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes.

Current understanding based on the effect of dietary lipid manipulation upon immune system function indicates that fatty acids are involved in the modulation of the immune response through different and complex pathways. Reduction of several immune parameters by fatty acid action may be applied in the treatment of diseases characterised by an overactivation of the immune system. As a consequence, a reduction of host resistance against infectious agents has been reported in animals fed dietary lipids. The present study confirms the action of dietary lipids on the survival of mice infected with the pathogenic bacterium Listeria monocytogenes. A significant increase in peritoneal cells from mice fed a hydrogenated coconut oil diet was found, while a significant reduction of bacterial recovery from spleens of these mice was observed in this group. In addition, both eicosanoid and phospholipase inhibitors did not promote any modification of lymphocyte proliferation from mice fed olive oil or fish oil.

Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes

Current understanding based on the effect of dietary lipid manipulation upon immune system function indicates that fatty acids are involved in the modulation of the immune response through different and complex pathways. Reduction of several immune parameters by fatty acid action may be applied in the treatment of diseases characterised by an overactivation of the immune system. As a consequence, a reduction of host resistance against infectious agents has been reported in animals fed dietary lipids. The present study confirms the action of dietary lipids on the survival of mice infected with the pathogenic bacterium Listeria monocytogenes. A significant increase in peritoneal cells from mice fed a hydrogenated coconut oil diet was found, while a significant reduction of bacterial recovery from spleens of these mice was observed in this group. In addition, both eicosanoid and phospholipase inhibitors did not promote any modification of lymphocyte proliferation from mice fed olive oil or fish oil.

The effect of dietary lipid manipulation on murine splenic lymphocytes apoptosis and heat shock protein over expression.

In this study, we kept BALB/c mice on a hyperlipidic diet for 120 days and then assessed the predisposition to apoptosis and the appearance of heat shock protein (Hsp) on splenic lymphocytes. By immunoblot analysis, bands corresponding to Hsp 60 and Hsp 70 in cells from mice kept on a saturated fatty acid diet showed a greater expression already after 1 month while two other bands, which correspond to Hsp 25 and Hsp 27, were slightly present after 1 month of treatment. In cells from mice kept on a diet rich in unsaturated fatty acid, there was a marked expression of Hsp 25 and Hsp 27 after only 30 days of treatment, which was maintained constant for up to 4 months; while for bands corresponding to Hsp 60 and Hsp 70, a significant minor signal was only detectable after 2-4 months from the beginning of the treatment. Splenic lymphocytes from animals kept on a lipidic diet containing saturated fatty acids were more susceptible to death by apoptosis, while cells of animals treated with unsaturated fatty acid were shown to be more resistant.

The effect of dietary lipid manipulation on murine splenic lymphocytes apoptosis and heat shock protein over expression

In this study, we kept BALB/c mice on a hyperlipidic diet for 120 days and then assessed the predisposition to apoptosis and the appearance of heat shock protein (Hsp) on splenic lymphocytes. By immunoblot analysis, bands corresponding to Hsp 60 and Hsp 70 in cells from mice kept on a saturated fatty acid diet showed a greater expression already after 1 month while two other bands, which correspond to Hsp 25 and Hsp 27, were slightly present after 1 month of treatment. In cells from mice kept on a diet rich in unsaturated fatty acid, there was a marked expression of Hsp 25 and Hsp 27 after only 30 days of treatment, which was maintained constant for up to 4 months; while for bands corresponding to Hsp 60 and Hsp 70, a significant minor signal was only detectable after 2–4 months from the beginning of the treatment. Splenic lymphocytes from animals kept on a lipidic diet containing saturated fatty acids were more susceptible to death by apoptosis, while cells of animals treated with unsaturated fatty acid were shown to be more resistant.

The effect of dietary lipid manipulation on the uptake of [3H]-triolein by tissues of the rat.

The effect of dietary lipid manipulation on the uptake of [3H]-triolein by tissues of the rat.

Effects of Dietary Lipid Manipulation upon Graft vs Host and Host vs Graff Responses in the Rat

The popliteal lymph node (PLN) assay was used to establish whether dietary lipids with differing fatty acid compositions could affect cell-mediated immunity in the rat. Weanling rats were fed for 4 weeks on a low-fat (2.5% by weight; LF) diet or on diets containing 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO), or menhaden (fish) oil (MO). Feeding the MO diet suppressed the graft vs host response compared with feeding the LF, HCO, SO, or EPO diets, while feeding the OO diet suppressed this response compared with feeding the LF or EPO diets. Feeding the MO diet suppressed the host vs graft response compared with feeding each of the other diets. Following the graft vs host reaction, PLN lymphocytes from animals fed the MO diet had significantly lower levels of expression of LFA-1 and CD2 compared with PLN lymphocytes from animals fed the LF diet; furthermore, they had lower levels of expression of T-cell receptor (TcR), CD4, CD8, LFA-1, and CD2 compared with lymphocytes from animals fed some, and in the case of CD2 each, of the other high-fat diets, Feeding the MO diet resulted in a lower proportion of cells expressing the interleukin-2 receptor, indicating an inhibition of lymphocyte activation, and a lower proportion of CD16 +/CD3 - cells, indicating a decrease in the proportion of NK cells within the PLN. Following the host vs graft reaction, PLN lymphocytes from animals fed the MO diet had significantly lower levels of expression of TcR and CD8 compared with lymphocytes from animals fed each of the other diets; furthermore, they had lower levels of expression of CD4, CD2, and LFA-1 compared with lymphocytes from animals fed the LF, HCO, OO, or SO diets. These observations indicate that the smaller PLN size of animals fed the MO diet results from an inhibition of activation and subsequent proliferation of cells within the node and perhaps also a suppression of movement of cells from the bloodstream to the PLN, due to decreased level of expression of adhesion molecules. These lowered levels of expression might be due to an inhibitory effect of the n-3 polyunsaturated fatty acids found in MO upon components of the signal transduction pathways involved in lymphocyte activation or upon expression of the genes for the surface molecules or both.

The effects of dietary lipid manipulation on the production of murine T cell-derived cytokines.

Lymphocytes play an important part in the development and progression of a number of autoimmune and inflammatory disorders, which are characterized by the presence of activated T cells and cytokines at the site of tissue injury and in the circulation. There has been considerable interest in using dietary polyunsaturated fatty acids (PUFA), particularly the n-3 PUFA found in fish oils, in the therapy of these conditions; such therapies aim, primarily, to suppress T-lymphocyte activity. While several studies have investigated the effects of fatty acids on the production of monocyte- and macrophage-derived cytokines, few have investigated their effects on the production of T cell-derived cytokines. Each of these studies have been restricted to IL-2 and have produced results which are not entirely clear. Moreover, there have been no studies to investigate the effects of dietary lipids other than fish oils on IL-2 production or the effects of dietary lipids on lymphokines other than IL-2. To investigate the effects of dietary lipid manipulation on the production of IL-2, IL-4, IL-10 and IFN-gamma by lymphocytes, mice were fed for 8 weeks on a low fat (LF) diet or one of 4 high fat diets, which contained 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO) or menhaden oil (MO). Culture medium of lymphocytes from mice fed the OO or SO diets contained significantly more IL-2 than that of lymphocytes from mice fed the LF or HCO diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Dietary Lipid Manipulation upon Inflammatory Mediator Production by Murine Macrophages

This study investigated the effects of feeding mice lipids with different fatty acid compositions upon the ability of stimulated macrophages to produce inflammatory mediators. Weanling mice were fed for 8 weeks on a low-fat (LF; 2.5% by weight) diet or on diets containing 20% by weight of hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), or menhaden (fish) oil (MO). Thioglycollate-elicited peritoneal macrophages were isolated. Macrophages isolated from MO-fed mice produced less PGE2, 6-keto-PGF1a, TXB2, and interleukin-6 in response to lipopolysaccharide (LPS) stimulation than those from mice fed each of the other diets. Macrophages from mice fed the OO, SO, or MO diets produced less tumor necrosis factor a in response to LPS stimulation than those from mice fed the LF or HCO diets. There was no effect of dietary lipid manipulation upon the production of interleukin-1 by LPS-stimulated macrophages. Macrophages from mice fed the MO diet produced more superoxide and hydrogen peroxide in response to phorbol ester stimulation than those from mice fed each of the other diets. In response to unopsonized zymosan, macrophages from mice fed the SO or MO diets produced more hydrogen peroxide than macrophages from mice fed the other diets. LPS-stimulated nitric oxide production was greater from macrophages from OO-, SO-, or MO- fed mice than from those fed the LF or HCO diets. Thus, the nature of the lipid consumed in the diet has significant effects upon the production of a variety of inflammatory mediators by macrophages. The most potent effect is caused by fish oil consumption. Possible mechanisms by which dietary fatty acids, particularly the n-3 polyunsaturated fatty acids found in fish oils, could affect mediator production by macrophages are described. The clinical relevance of such effects is discussed.

The effect of fatty acids on leucocyte subsets and proliferation in rat whole blood

Polyunsaturated fatty acids (PUFA) have been shown to suppress immune cell functions in vitro. Dietary studies investigating the effects of PUFA-containing oils on lymphocyte functions have yielded contradictory findings; such studies are difficult to compare since there are many variations in protocols. The present study investigated the effects of exogenously added fatty acids on proliferation of leucocytes to whole blood in vitro and the effects of feeding diets containing oils rich in saturated fatty acids, monounsaturated fatty acids, n-6 PUFA or n-3 PUFA on rat leucocyte proliferation in whole blood and on receptor and surface marker expression by peripheral blood leucocytes. When added exogenously to whole blood all fatty acids tested, except myristic acid, inhibited leucocyte proliferation; the greatest inhibition of proliferation was seen with arachidonic and eicosapentaenoic acids. To investigate the effects of dietary lipids on proliferation and surface marker expression by leucocytes, rats were fed for ten weeks on a low fat (LF) diet (approximately 2% fat by weight) or on one of five high fat diets, which contained 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Compared with feeding the LF, SO or EPO diets, the HCO, OO and MO diets suppressed the proliferation of leucocytes in whole blood at low concentrations of Con A. High fat feeding decreased the sensitivity of B-cells to LPS, but had no effect on the magnitude of the response to this mitogen. Dietary lipid manipulation had no effect on leucocyte subpopulations (T-cells, B-cells, CD4 + cells, CD8 + cells, monocytes/macrophages, natural killer cells) or on the expression of adhesion molecules (LFA-1, ICAM, CD2). The effects of dietary lipid manipulation on leucocyte proliferation are clearly very different from the effects of addition of single fatty acids to whole blood in vitro. This is likely to be due to alterations in blood triacylglycerol and cholesterol concentrations brought about by different dietary lipids, suggesting that dietary lipids have marked effects on leucocyte proliferation and that the use of the whole blood system may be a more physiological way of determining the effects of dietary lipids on immune function than the use of single exogenously added fatty acids with purified cells.

Effects of Dietary Lipid Manipulation upon Rat Spleen Lymphocyte Functions and the Expression of Lymphocyte Surface Molecules

Rats were fed for 12 weeks on a low fat (LF; 2.5% by weight) diet or on one of five high fat (20% by weight) diets; the latter contained hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Feeding the EPO or MO diets resulted in inhibition of mitogen-stimulated spleen lymphocyte proliferation compared with feeding any of the other diets; in addition, feeding the OO diet resulted in inhibition of proliferation compared with feeding the LF diet. Feeding the OO, EPO or MO diets resulted in inhibition of spleen lymphocyte natural killer (NK) cell activity compared with feeding the LF or HCO diets; feeding the SO diet resulted in inhibition of NK cell activity compared with feeding the HCO diet. There was no effect of dietary lipid manipulation upon the proportion of T-cells or of CD4+ or CD8+ cells in the spleen. The level of expression of CD2 on CD4+ and CD8+ spleen lymphocytes was decreased by MO feeding compared with feeding the LF, HCO, SO or EPO diets; OO feeding decreased the level of expression of CD2 on CD4+ spleen lymphocytes compared with feeding the LF diet. The level of expression of LFA-1 was decreased on both CD4+ and CD8+ spleen lymphocytes from animals fed the OO or MO diets compared with that on lymphocytes from animals fed some of the other diets. Following mitogenic stimulation the level of expression of CD8, CD2, ICAM-1, LFA-1 and the interleukin-2 receptor was lower on spleen lymphocytes from animals fed the MO diet and, for some of the markers, on those from animals fed the OO or EPO diets. These observations indicate that diets containing MO, OO and EPO exert immunomodulatory effects by influencing the expression of important molecules upon the lymphocyte surface. This may occur through effects on signal transduction pathways and/or gene expression.