| | Dietary effect of pomegranate seed oil on immune function and lipid metabolism in miceReceived 7 December 2004; accepted 1 March 2005. published online 13 October 2005. Abstract ObjectivesWe evaluated the effects of dietary pomegranate seed oil (PSO), which contains high levels of punicic acid (9c, 11t, 13c-octadecatrienoic acid), on immune function and lipid metabolism in C57BL/6N mice. MethodsMice were fed experimental diets containing 0%, 0.12%, or 1.2% PSO for 3 wk. ResultsNo significant differences were observed between growth patterns of the experimental groups. Splenocytes isolated from mice fed 0.12% or 1.2% PSO produced larger amounts of immunoglobulins G and M but not immunoglobulin A irrespective of stimulation with or without phorbol 12-myristate 13-acetate and the calcium ionophore A23187. Dietary PSO did not affect the percentages of B cells or CD4-positive or CD8-positive T cells in splenocytes. Levels of interleukin-4, interferon-γ, and tumor necrosis factor-α production from splenocytes were comparable among all dietary groups. Analysis of serum lipid parameters showed significant increases in serum triacylglycerol and phospholipid levels but not in total cholesterol in the PSO groups. Serum, liver, epididymal, and perirenal adipose punicic acid levels were high with increases in dietary PSO level. However, punicic acid was not detected in splenocytes for any dietary group. Interestingly, 9c, 11t-conjugated linoleic acid level could be detected in serum, liver, and adipose tissues in mice fed the 0.12% or 1.2% PSO diet. ConclusionsThese results suggest that PSO may enhance B-cell function in vivo.
Introduction  There are accumulating data indicating that dietary fat manipulates various immunologic functions. For example, modulation of dietary fat quality, such as dietary fat level and the balance of ω-6/ω-3 polyunsaturated fatty acids, strongly affects lymphocyte function [1], [2]. The balance of dietary fatty acids and of trace fatty acids in food components is also expected to influence immune function. Conjugated linoleic acid (CLA) is a generic term for the positional and structural isomers of octadecadienoic acid. CLA has been reported to exert various beneficial physiologic functions at extremely low dietary levels. Our previous study showed that CLA strongly promotes immunoglobulin (Ig) production and modulates the production of various cytokines in rat and mouse splenocytes [3], [4], [5], [6]. In addition, 10trans, 12cis-CLA promoted Ig production, whereas 9cis, 11trans-CLA promoted tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) production. These observations suggest that dietary conjugated polyunsaturated fatty acids exert potent and beneficial physiologic functions through their immunomodulatory effects. Further, pomegranate seed oil (PSO) contains large amounts of 9cis, 11trans, 13trans-conjugated linolenic acid (CLN), called punicic acid. Various CLNs have been shown to inhibit the growth of transplanted cancer cells or to exert cancer cell killing activity in vitro [7], [8], [9]. No evidence has yet been reported to suggest immunomodulatory functions of CLN. We studied the effects of dietary PSO on the function of splenocytes in mice. Materials and methods Pomegranate seed oil (fatty acid composition presented in Table 1) was prepared at the Plantech Research Institute (Yokohama, Japan), and soybean oil was purchased from Sigma (St. Louis, MO, USA). Male, 4-wk-old C57BL/6N mice (n = 24; Japan CLEA Inc., Tokyo, Japan) were fed a non-purified commercial pellet diet and given water ad libitum for 1 wk after their arrival. After acclimation, mice were assigned to one of three groups of eight animals each. Mice were kept at the Biotron Institute of Kyushu University (Fukuoka, Japan) under a 12-h light/12-h dark cycle (lights on from 8:00 am to 8:00 pm) in an air-conditioned room (20°C and 60% humidity under specific pathogen-free conditions). This experiment was carried out according to the guidelines for animal experiments of the Faculty of Agriculture and the Graduate Course, Kyushu University, and the Law (No. 105) and Notification (No. 6) of the Japanese Government. As presented in Table 1, experimental diets were manufactured according to AIN-93G standards [10] and contained 0%, 0.12%, or 1.2% PSO. At the end of the feeding period, mice were killed by exsanguination from the abdominal aorta under light anesthesia with diethyl ether. Immediately after excision, each tissue was weighed and lymphocytes were isolated from the spleen.
 | 16:0 | 3.1 | |
| 18:0 | 1.8 | |
| 18:1 (ω-9) | 5.4 | |
| 18:1 (ω-7) | 0.4 | |
| 18:2 (ω-6) | 5.3 | |
| 18:3 (punicic acid) | 83.1 | |
| 20:0 | 0.4 | |
| 20:1 | 0.5 | | | | |
Preparation of spleen lymphocytes was performed according to a method described previously [4] without removing adhesive cells, such as macrophages and mononuclear cells. Briefly, a cell suspension prepared from the spleen was rinsed three times with RPMI-1640 medium (Nissui, Tokyo, Japan). Then 5-mL aliquots of cell suspension were added to Lympholyte-mouse (Cedarlane, Hornby, Canada) to isolate the lymphocytes and again washed three times with RPMI-1640 medium. Lymphocytes were cultured at 2.5 × 106 cells/mL in RPMI-1640 medium containing 10% fetal bovine serum (Intergen, Purchase, NY, USA) with or without 8 nM phorbol 12-myristate 13-actate (PMA) and the calcium ionophore A23187 at 150 nM, followed by incubation at 37°C for 24 h. Measurement of Ig concentration in the cultured medium was performed by sandwich enzyme-linked immunosorbent assay. Rabbit anti-mouse IgA (Zymed, San Francisco, CA, USA), goat anti-mouse IgG (H+L; Zymed), and rabbit anti-mouse IgM (μ-chain specific; Zymed) were used to fix each Ig. These antibodies were diluted using 10% Block Ace (Dainihon Pharmaceutical Co., Osaka, Japan), added to 96-well plates, and incubated for 1 h at 37°C. Aliquots containing 300 μL of 10% (25% for IgE) Block Ace were added and kept at 4°C overnight, and then samples (50 μL) were added to each well for 1 h at 37°C. Each well was treated with a solution of peroxidase (POD)–conjugated goat anti-mouse IgA (Zymed), POD-conjugated goat anti-mouse IgG (H+L; Zymed), or POD-conjugated rabbit anti-mouse IgM (Zymed) to detect the respective Ig and incubated for 1 h at 37°C (20 min at 4°C for IgE). Plates were rinsed with phosphate buffered saline containing 0.05% polyethylene sorbitan monolaurate (Nacalai Tesque, Kyoto, Japan) between each step. Then a 10:9:1 mixture of 1.8 mmol/L of hydrogen peroxide in 0.2 mol/L of citrate buffer (pH 4.0), H2O, and 11.7 mmol/L of 2,2′-azinobis (3-ethylbenzothiazoline sulfonic acid) was added. Absorbance at 415 nm was measured after the addition of 160 mmol/L of oxalic acid to stop the coloring reaction. We measured levels of interleukin-4 (IL-4), TNF-α, and IFN-γ from the supernatants of spleen lymphocytes cultured with PMA and A23187. TNF-α and IFN-γ levels were measured by sandwich enzyme-linked immunosorbent assay as reported previously [4]. Briefly, rabbit anti-mouse/rat IFN-γ (BioSource), anti-mouse TNF-α (Endogen, Woburn, Sunnyvale, MA, USA), or anti-mouse IL-4 (BD Bioscience, Franklin Lakes, NJ, USA; 1:500 dilution) were used to fix these cytokines for 1 h at 37°C (overnight at 4°C for IL-4). Then blocking was performed using 25% Block Ace at 37°C for 1 h. In the following step, each well was treated with 50 μL of appropriate cultured supernatant for 2 h at 37°C and then the plate was treated with a diluted solution of biotinylated anti-mouse IFN-γ (Genzyme, Cambridge, MA, USA; 1:500 dilution), biotinylated anti-mouse/rat TNF-α (Genzyme; 1:250 dilution), or biotinylated anti-mouse/rat IL-4 (BD Bioscience) for 1 h at 37°C. Streptavidin-conjugated POD (Zymed) diluted with 10% Block Ace was added to each well and incubated for 1 h at 37°C. Plate washing between each step and the coloring reaction was performed as described for the Ig measurement protocol. The coloring step was performed by the same method as described for quantification of Ig. CD45R (a B-cell marker), CD4, and CD8 (T-cell subpopulation markers) cell surface expressions were analyzed by flow cytometry as reported previously [4]. After isolation of lymphocytes from the spleen, cells were washed three times with RPMI-1640 medium and treated with phosphate buffered saline containing 3% bovine serum albumin for 1 h at 37°C. Cells were divided into two groups (1.0 × 106 cells each), and then one was exposed to rat phycoerythrin-conjugated monoclonal anti-mouse CD45R (clone RA3-6B2, Caltag Laboratories, Burlingame, CA, USA) and the other was double stained with rat fluorescein isothiocyanate–conjugated monoclonal anti-mouse CD4 (clone CT-CD4, Caltag Laboratories) and rat phycoerythrin-conjugated monoclonal anti-mouse CD8b (clone CT-CD8b, Caltag Laboratories). All antibody reactions were performed on ice for 1 h, and cells were washed three times with phosphate buffered saline after antibody treatment. Samples were subjected to flow cytometry (FACSCalibur, Becton Dickinson, Sunnyvale, CA, USA) and 104 cells were analyzed to determine the percentages of CD45R-, CD4-, and CD8-positive lymphocytes. Serum triacylglycerols (TG), total cholesterol, and phospholipids (PLs) were measured using commercial kits (Wako, Osaka, Japan) according to the manufacturer’s protocol. Total lipids were extracted according to the method described by Folch et al. [11] using a chloroform/methanol (2:1 by volume) mixture. After extraction, transmethylation was performed as reported previously [12]. Briefly, total lipids were resolved into sulfuric acid/methanol/dimethylsulfoxide (1:115:115 by volume) and kept at 80°C for 2 h. Methylated fatty acids were re-extracted using hexane, and fatty acid composition analysis was performed by gas liquid chromatography (GC-14B Shimadzu Kyoto) equipped with a Supelcowax-10 column (0.32 mm × 60 m, film thickness 0.25 μm; Supelco Inc., Bellefonte, PA, USA). Column temperature was kept at 220°C and the detector and injector temperatures were set at 250°C. Data were analyzed by analysis of variance and Fisher’s Protected Least Significant Difference (PLSD) test to evaluate the significance of differences. All experimental data are shown as means ± standard errors, and values not sharing a common superscript letter are significantly different at P < 0.05. Results Table 2 presents the effects of PSO on the growth parameters of the mice. There were no significant differences in body weight or tissue weight among any of the dietary groups. There were no significant differences in food intake during the experimental period across dietary groups (data not shown). Table 3 presents the dietary effects of PSO on Ig production by spleen lymphocytes. Dietary PSO did not affect IgA productivity at any dose examined irrespective of PMA and A23187 stimulation. The results indicated that IgM production in splenocytes was significantly modulated by PMA and A23187 stimulation (analysis of variance). Analysis of variance showed that diet significantly affected IgG and IgM production, and post hoc testing showed that dietary PSO significantly promoted the production of these Ig classes. Levels of IgG and IgM production by splenocytes were comparable between the 0.12% and 1.2% PSO groups. There were no significant differences in interaction of diet and stimulation (PMA plus A23187) for all Ig classes. Serum IgA, IgG, and IgM levels were comparable across all dietary groups when serum was collected after 1, 2, and 3 wk of feeding (data not shown). Cytokine production was not detected in any of the culture supernatants from lymphocytes without PMA and A23187 stimulation. Table 4 lists the effects of dietary PSO on cytokine production from spleen lymphocytes stimulated with PMA and A23187. Dietary PSO did not affect the production of IL-4 or IFN-γ, representative cytokines produced by helper T-cell types 1 (Th1) and 2 (Th2), respectively. In addition, TNF-α production was also comparable across dietary groups. To assess the percentage of B cells in the entire spleen lymphocyte population, the percentage of CD45R+ was measured. Percentages of B cells among mouse splenocytes were comparable across dietary groups. Results showed the effects of dietary PSO on the percentages of CD4+ and CD8+ T cells. There were no significant differences in CD4+ or CD8+ T-cell percentages among any of the dietary groups (data not shown). Next, we evaluated serum TG, total cholesterol, and PL levels as representative serum lipid parameters (Table 5). All lipid parameters measured showed slight increases in a PSO dose-dependent manner. Although no significant differences were detected in total cholesterol level among the dietary groups, TG and PL levels in the PSO group were significantly different from those in the control group. Table 6, Table 7, Table 8, Table 9, Table 10 presents the fatty acid compositions of the liver, serum, adipose tissue, and splenocytes, respectively. Punicic acid level was increased in PSO-fed mice in a PSO dose-dependent manner. However, no punicic acid was detected in splenocytes from any dietary group. Accumulation of punicic acid was highest in adipose tissue. PSO dose-dependent accumulation of 9c, 11t-CLA was observed in the serum, liver, and adipose tissues with increasing level in the diet. In liver or serum, the 9c, 11t-CLA level exceeded that of punicic acid. No 9c, 11t-CLA was detected in splenocytes at any dose of dietary PSO examined in the present study (Table 10). Discussion PSO contains more than 80% 9c, 11t, 13c-octadecatrienoic acid, called punicic acid (Table 1). PSO has been shown to suppress chemically induced carcinogenesis and exert antiangiogenic activity [7], [8], [9]. Recent studies of conjugated polyunsaturated fatty acids have indicated that dietary CLA modulates immunologic function in rats, mice, chicks, pigs, and humans [3], [4], [5], [6], [13], [14], [15], [16], [17]. These results suggested that dietary conjugated fatty acids have significant beneficial effects on immunologic function. However, little information is available about the immunomodulatory function of conjugated trienoic acid. We evaluated the effects of PSO on immune function and lipid metabolism in C57BL/6N mice. In the present study, serum TG and PL concentrations were significantly higher in the PSO groups than in the control group, and PSO did not affect the weight of adipose tissue. CLA decreases body fat and serum TG level in mice, but recent results reported by Koba et al. [18] showed that CLA (a mixture of various isomers with conjugated dienoic or trienoic double bonds) increased serum TG level in rats [18]. Specifically, 9c, 11t, 13t-octadecatrienoic acid occurs in karela seed oil and increased serum TG and total cholesterol levels compared with linseed oil, which is rich in α-linolenic acid [19]. Thus, serum TG level should be increased when certain CLNs are administered orally. Modulation of dietary fatty acid composition manipulates Ig production by splenocytes [20], [21], [22]. In addition, dietary CLA is a potent enhancer of Ig production [3], [4], [5], [6], [7]. Therefore, polyunsaturated fatty acids including conjugated double bonds, such as CLN, are expected to enhance Ig production. Results of the present study indicated that dietary PSO significantly enhanced IgG and IgM production by splenocytes. As presented in Table 6, Table 7, Table 8, Table 9, Table 10, 9c, 11t-CLA was detected in the serum, liver, and adipose tissue of mice fed PSO. Dietary CLN has been shown to be converted to CLA in rats, and CaCo2, a human colon carcinoma cell line, also converted CLN to CLA [23], [24]. What about the relation between promotion of Ig production by dietary PSO and bioconversion of PSO into 9c, 11t-CLA? Our previous study showed that 10t, 12c-CLA, but not 9c, 11t-CLA, was an active isomer to enhance Ig production in vivo [4]. In addition, we detected neither punicic acid nor 9c, 11t-CLA in splenocytes from mice fed PSO. These results indicated that incorporation of punicic acid or CLA into splenocytes is not essential for promotion of Ig production, but we can not deny the possibility that very small quantities of PSO or its metabolite (such as elongation, desaturation, or β-oxidation) in splenocytes, which are not detected by gas chromatographic analysis, are the active component. Moreover, it is assumed that 9c, 11t-CLA produced from punicic acid is not an active isomer to promote Ig production. When compared with the effect of dietary 10t, 12c-CLA and PSO, 10t, 12c-CLA promoted IgA production [4], whereas PSO did not (Table 3). We previously showed that 10t, 12c-CLA promoted Ig production with modulation of balance for lymphocyte population [6], whereas dietary PSO did not modulate lymphocyte population balance. Thus, the promotive effect of Ig by dietary PSO might be exerted by a mechanism different from 10t, 12c-CLA. Dietary fatty acid composition also modulates the balance of the T-cell population [25], and our previous study showed that dietary 10t, 12c-CLA increased the B-cell population with promotion of Ig production in mouse splenocytes [4]. To examine the effects of PSO on the B-cell ratio and T-cell subpopulation in spleen lymphocytes, we measured the lymphocyte-specific surface markers CD45R (B cell), CD4 (Th cell), and CD8 (killer T cell). PSO did not affect the percentages of B- or T-cell subpopulations. In addition, Th cells were roughly classified into Th1 and Th2 cells, and this classification was characterized as the type of cytokines secreted from T cells. As representative cytokines, IL-2, IL-12, and IFN-γ are produced by Th1 cells, whereas IL-4, IL-5, IL-10, and IL-13 are produced by Th2 cells. We measured IL-4, IFN-γ, and TNF-α productivity of splenocytes. The results showed that PSO did not affect the production of any of these cytokines and indicated that dietary PSO did not modulate the Th1/Th2 balance in mouse splenocytes. Previous studies have shown that dietary octadecatrienoic acid without conjugated double bonds does not modulate the balance of the T-cell population (CD4+/CD8+ or Th1/Th2) [26]. Taken together, these observations indicated that dietary PSO does not influence the balance of the B- or T-lymphocyte population, and promotion of Ig production by dietary PSO cannot be explained by modulation of the B- and T-cell population balance in splenocytes. 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MEDLINE a Department of Biochemistry and Applied BioScience, Faculty of Agriculture, Miyazaki University, Miyazaki, Japan b Laboratory of Food Chemistry, Division of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, Fukuoka, Japan c Plantech Research Institute, Yokohama, Japan d Department of Bioresource Science, Faculty of Agriculture, Tamagawa University, Tokyo, Japan  Corresponding author. Tel./fax: +81-985-58-7209.
PII: S0899-9007(05)00233-9 doi:10.1016/j.nut.2005.03.009 © 2006 Elsevier Inc. All rights reserved. | |
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