Department of Medical Education and Research, Changhua Christian Hospital, Changhua, Taiwan.
JPEN J Parenter Enteral Nutr. 2012 Nov;36(6):741-9. doi: 10.1177/0148607111429793. Epub 2012 Jan 23.
Arginine deficiency and chronic inflammation may cause immune dysfunction. The authors previously showed that a pharmacological dose of parenteral arginine facilitates ornithine rather than nitric oxide production in subacute peritonitis. Herein, they investigated the effects of different doses of parenteral arginine supplementation on immunocytic subpopulation distribution and function.
Male Wistar rats that underwent cecal punctures for induction of subacute peritonitis were infused with conventional parenteral nutrition solution (1.61% of total calories as arginine) or solutions supplemented with low-, medium-, or high-dose arginine (2.85%, 4.08%, and 6.54% of total calories, respectively) for 7 days. Distributions of T cells, B cells, and monocytes/macrophages and cytokine productions of peripheral blood lymphocytes (PBLs) and splenocytes were analyzed.
There were no significant differences in circulating white blood cell numbers and serum tumor necrosis factor (TNF)-α and interferon (IFN)-γ concentrations among groups. Serum nitrate/nitrite (NOx) and interleukin (IL)-2 levels were significantly decreased by arginine in a dose-dependent manner. Animals supplemented with parenteral arginine had significantly decreased productions of concanavalin (Con) A- and lipopolysaccharide (LPS)-stimulated TNF-α in PBLs and splenocytes, spontaneous IL-6 and LPS-stimulated IFN-γ in PBLs, and LPS-stimulated IL-6 in splenocytes. In addition, low-dose arginine significantly increased production of spontaneous IFN-γ in PBLs and splenocytes. High-dose arginine significantly increased spontaneous TNF-α, and Con A stimulated IL-4 and IL-6 in PBLs.
Parenteral arginine administration at approximately 4% of total calories may alter PBLs and splenocytic immunity, and >6% of total calories might not be of benefit in rats with subacute peritonitis.
精氨酸缺乏和慢性炎症可能导致免疫功能障碍。作者先前表明,药理剂量的外源性精氨酸有利于鸟氨酸而不是一氧化氮的产生,从而在亚急性腹膜炎中发挥作用。在此,他们研究了不同剂量的外源性精氨酸补充对免疫细胞亚群分布和功能的影响。
雄性 Wistar 大鼠接受盲肠穿刺术以诱导亚急性腹膜炎,并接受常规肠外营养溶液(总热量的 1.61%为精氨酸)或补充低、中、高剂量精氨酸(总热量的 2.85%、4.08%和 6.54%)的溶液进行 7 天输液。分析外周血淋巴细胞(PBL)和脾细胞的 T 细胞、B 细胞和单核细胞/巨噬细胞分布以及细胞因子产生情况。
各组间循环白细胞数量、血清肿瘤坏死因子(TNF)-α和干扰素(IFN)-γ浓度无显著差异。精氨酸呈剂量依赖性显著降低血清硝酸盐/亚硝酸盐(NOx)和白细胞介素(IL)-2水平。补充外源性精氨酸的动物脾细胞和 PBL 中刀豆蛋白 A(Con)A 和脂多糖(LPS)刺激的 TNF-α产生、PBL 中自发的 IL-6 和 LPS 刺激的 IFN-γ产生以及 LPS 刺激的脾细胞中 IL-6 产生均显著降低。此外,低剂量精氨酸显著增加了 PBL 和脾细胞中自发 IFN-γ的产生。高剂量精氨酸显著增加了 PBL 中自发 TNF-α和 Con A 刺激的 IL-4 和 IL-6,以及 LPS 刺激的脾细胞中 IL-6 的产生。
约占总热量 4%的肠外精氨酸给药可能改变 PBL 和脾细胞免疫,而在亚急性腹膜炎大鼠中,超过 6%的总热量可能无益。