Metabolism of [3H]arachidonic acid by n-3 polyunsaturated fatty acid-enriched piglet alveolar macrophages.

The metabolism of [3H]arachidonic acid (3H-AA) by control and omega-3 polyunsaturated fatty acid (n-3 PUFA)-enriched piglet alveolar macrophages (AM) was studied after a 4 and 24 h labeling period. 3H-AA metabolites were separated by gradient HPLC. Incorporation of exogenous 3H-AA for either 4 or 24 h was similar for n-3 PUFA-enriched AM compared with control AM. Calcium ionophore (A23187, 10 microM) stimulated a greater release of 3H-AA from n-3 PUFA-enriched AM compared with control AM. Furthermore, AM labeled for 24 h had a lower spontaneous release and higher stimulated release than those labeled for only 4 h. The major 3H-AA metabolites detected in AM supernatants were PGF2 alpha, LTB4, and 5-HETE. Significant amounts of 3H-PGE2 were observed in the supernatants of those cells labeled for 24 h, but not 4 h. The absence of 3H-TXB2 was notable, since enzyme immunoassay detected significant quantities of this AA metabolite in all of the stimulated cell supernatants. From these data we conclude that n-3 PUFA enrichment of piglet AM alters the metabolism of recently incorporated 3H-AA and that the metabolism of labeled AA may not parallel endogenous AA.

Fish oils lower rat plasma and hepatic, but not immune cell alpha-tocopherol concentration.

These studies were designed to measure the impact of different fish oil sources of dietary (n-3) polyunsaturated fatty acid on the alpha-tocopherol content of rat immune cells. In the first experiment, rats were fed diets containing either lard, corn oil, menhaden fish oil or cod liver oil. In the second study, sardine fish oil replaced corn oil. Dietary fat source did not significantly influence body weights or the yield of immune cells in either study. In both studies, plasma and liver alpha-tocopherol concentrations were significantly lower in (n-3) polyunsaturated fatty acid-fed rats than in rats fed lard. In the first study, immune cell alpha-tocopherol concentrations followed those observed in the plasma and liver. These concentrations closely paralleled the amount of RRR-alpha-tocopheryl acetate added to diets and not the total vitamin E present, which was the same for all treatment groups. However, in the second study, alpha-tocopherol concentration of immune cells was not significantly different among rats fed lard, menhaden fish oil, and sardine fish oil. In that study both the amount and form of vitamin E were carefully balanced across dietary treatment groups. In conclusion, despite having similar amounts of (n-3) polyunsaturated fatty acids, two out of three fish oils tested did not lower immune cell alpha-tocopherol concentration even in the face of significantly reduced plasma and liver alpha-tocopherol concentrations.

Maternally-supplied fish oil alters piglet immune cell fatty acid profile and eicosanoid production.

This study was designed to examine the incorporation of omega-3 (n-3) fatty acids into the immune tissues of pigs nursing fish oil-fed sows and to determine the effect of maternal dietary n-3 consumption on in vitro immune cell eicosanoid production. On day 107 of gestation, 12 sows were randomly allotted to a diet containing either 7% menhaden fish oil (MFO) or lard (LRD). The fatty acid profile of serum, liver, thymus, splenocytes and alveolar macrophages (AM) of 18-21-day-old pigs was significantly affected by the fat source provided to the sow. Arachidonic acid (20:4n-6) content was typically reduced by more than 50% in MFO as compared with LRD pigs. In MFO pigs, eicosapentaenoic acid (20:5n-3) was the major n-3 polyunsaturated fatty acid, and its levels matched or exceeded those of arachidonic acid. Basal release of prostaglandin E, thromboxane B and leukotriene B by AM was 60-70% lower in MFO vs. LRD pigs. However, when these immune cells were stimulated with calcium ionophore A23187, release of leukotriene B was similar in MFO and LRD pigs. In conclusion, substituting MFO for LRD in a sow's late-gestation and lactation diet greatly elevated the content of n-3 fatty acids in the nursing pig immune cells and generally reduced in vitro eicosanoid release by pig immune cells.

Enrichment of omega-3 fatty acids in suckling pigs by maternal dietary fish oil supplementation.

This study was designed to determine whether substituting menhaden fish oil (FO) for lard (LA) in a practical sow diet was a suitable method for enriching newborn pigs with omega-3 polyunsaturated fatty acids (n-3 PUFA). On d 107 of gestation, 18 crossbred sows were randomly allotted to one of three experimental diets, in which FO was substituted for LA at 0, 3.5, and 7% of the diet. On d 1, 7, 14, and 21 after farrowing samples of milk and serum from the sows and pig serum were collected for fatty acid analysis. The content of n-3 PUFA in the serum of sows fed FO increased six-fold over that in serum of LA-fed sows P < .0001). Feeding FO decreased the levels of arachidonic acid in maternal serum by approximately 50% (P < .0001). Similar changes were reflected in the fatty acid profiles of sow's milk. Pig serum n-3 PUFA levels were elevated over 5- and 10-fold within 24 h of birth in those litters born to sows fed 3.5 and 7% fish oil, respectively. Eicosapentaenoic acid levels in pig serum increased linearly (P < .01) during the first 2 wk postnatally in pigs suckling FO-feds sows and accounted for as much as 12% of the total fatty acids present on d 21. In conclusion, we have demonstrated that feeding FO to sows during late gestation and lactation enriches the newborn pig with n-3 PUFA.

Dietary n-3 fatty acids reduce antibody-dependent cell cytotoxicity and alter eicosanoid release by chicken immune cells.

The overall goal of the present study was to determine whether the incorporation of n-3 fatty acids into poultry rations would alter the immune response of broiler chickens. Female broiler chicks were fed a corn and soybean meal-based diet to which one of four dietary fats were added: lard (LA), corn oil (CO), flaxseed oil (SO), or menhaden fish oil (FO). The latter two fat sources are rich in n-3 polyunsaturated fatty acids (PUFA). Enriching the diet with n-3 PUFA did not alter the primary or secondary antibody response of broiler chickens to sheep red blood cells. Dietary fat source had no effect on antibody-dependent cell cytotoxicity (ADCC) by peripheral blood leukocytes, but ADCC by splenocytes was 50% lower in chickens fed SO and FO compared with LA and CO (P less than .005). As expected, the fatty acid profile of the isolated immune cells reflected the fatty acid composition of the dietary fats fed. Basal release and calcium ionophore (A23187)-stimulated (10 microM) release of thromboxane B were significantly lower (P less than .05) in the SO and FO groups compared with the LA and CO groups. Total leukotriene B release was not significantly altered by dietary fat source. In conclusion, feeding broiler chickens diets rich in n-3 PUFA reduced ADCC of splenocytes and altered eicosanoid production by isolated immune cells.

Dietary (n-3) fatty acid and vitamin E interactions in rats: effects on vitamin E status, immune cell prostaglandin E production and primary antibody response.

To examine the interaction between dietary fat and vitamin E at the level of the rat immune system, a 2 x 3 factorial study was designed. Weanling female Sprague Dawley rats were fed for 8-9 wk diets that contained either corn oil (CO diet) or fish oil (FO diet) and one of three levels (30, 300, 900 mg/kg) of all-rac-alpha-tocopheryl acetate. At the lowest level of dietary vitamin E, alpha-tocopherol content of splenocytes from FO-fed rats was approximately 40% lower (P less than 0.05) than in those from CO-fed rats. Supplementation with all-rac-alpha-tocopheryl acetate elevated alpha-tocopherol in splenocytes from FO-fed rats but not in those from CO-fed rats, and reduced the relative proportion of arachidonic acid and eicosapentaenoic acid in the serum of CO-fed and FO-fed rats, respectively. Prostaglandin E production by isolated immune cells was not affected by all-rac-alpha-tocopheryl acetate supplementation. However, feeding the FO diet consistently reduced prostaglandin E synthesis by 70-80% as compared with the CO diet. Antibody production against sheep RBC was highest in rats fed the FO diet supplemented with 900 mg all-rac-alpha-tocopheryl acetate/kg of diet. However, antibody response was not directly correlated to diet-induced changes in immune cell prostaglandin E production or alpha-tocopherol content. Our data suggest that there are significant interactions between vitamin E and (n-3) fatty acids that affect the immune system and that further research in this area is warranted.

Effect of dietary fats on the fatty acid compositions of serum and immune tissues in chickens.

The purpose of the present study was to measure the effect of dietary fat source on the fatty acid composition of immune cells in chickens. One-day-old female chicks were fed corn and soybean meal-based diets containing 7% of either lard, corn oil, canola oil, linseed oil (LO), or menhaden fish oil (FO). After being fed experimental diets for 3 to 4 wk, samples of serum, thymus glands, bursa of Fabricius glands, and splenocytes were collected. All samples were frozen and stored at -80 C until lipid analysis. Results indicate that the fatty acid composition of the sera and immune tissues of chickens reflected the fat in the diet. The relative content of long-chain polyunsaturated fatty acids varied considerably among immune tissues, with, from greatest to least, spleen, bursa, and thymus. The young chick demonstrated a substantial capacity to elongate and desaturate linoleic (C18:2n-6) and alpha-linolenic acids (C18:3n-3). Feeding chicks fats rich in n-3 fatty acids (e.g., LO or FO) decreased significantly (P less than .05) the level of arachidonic acid (C20:4n-6) present in the serum and immune tissues by 50 to 75%. The levels of eicosapentaenoic acid (EPA, C20:5n-3) and docosahexaenoic acid (DHA, C20:6n-3) were substantially increased (P less than .05) by FO and LO feeding. However, LO, which is rich in C18:3n-3, was generally only one-half to one-quarter as effective as FO in elevating EPA and DHA levels in immune tissues. The implications for these changes in serum and immune tissue fatty acid profiles are discussed briefly.

Effect of dietary fat source on antibody production and lymphocyte proliferation in chickens.

The purpose of the present study was to assess the effect of fat source on the immune response of chickens. One-day-old pullets were fed corn and soybean meal-based diets containing 7% by weight one of the following fat sources: lard, corn oil, canola oil, linseed oil (LO), or fish oil (FO). After being fed experimental diets for 3 wk, humoral and cellular immune responses were assessed. Chicks were injected with SRBC and antibody titers were measured, 7 days later, by hemagglutination. Concanavalin A (Con A), pokeweed mitogen (PWM), or lipopolysaccharide (LPS)-stimulated proliferation of splenocytes was assessed by [3H]thymidine incorporation. Results demonstrated that antibody titers in FO-fed chicks were higher (P less than .005) compared with titers in chicks fed the other fat sources. The proliferative response to Con A and PWM were 30 to 50% lower (P less than .13 and P less than .05, respectively) in chicks fed the oils rich in omega-3 fatty acids, LO and FO. The response to LPS was poor. The effect of dietary fats source on lymphocyte proliferation was completely abrogated when autologous chicken serum was excluded from the culture medium. Fat source also seemed to affect growth and feed intake of the chickens. In conclusion, dietary fat source has a significant impact on the immune response of chickens.