Institute and Department of Physiology and Immunology, Faculty of Medicine, Josip Juraj Strossmayer University of Osijek, J. Huttlera 4, HR-31000 Osijek, Croatia.
Scientific Center of Excellence for Personalized Health Care, Josip Juraj Strossmayer University of Osijek, Trg Svetog Trojstva 3, HR-31000 Osijek, Croatia.
Cell Physiol Biochem. 2024 Feb 27;58(1):83-103. doi: 10.33594/000000684.
BACKGROUND/AIMS: Unrestricted increased table salt (NaCl) intake is associated with oxidative stress and inflammation, leading to endothelial dysfunction and atherosclerosis. However, data on salt-induced immunomodulatory effects in the earliest phase of salt loading are scarce.
In the present study, an animal model of short-term salt loading was employed, including male Sprague Dawley rats consuming a high-salt diet (HSD; 4% NaCl) or standard laboratory chow (low-salt; LSD; 0.4% NaCl) during a 7-day period. The contribution of angiotensin II (ANGII) suppression was tested by adding a group of rats on a high-salt diet receiving ANGII infusions Samples of peripheral blood/mesenteric lymph node leukocytes, brain blood vessels, and serum samples were processed for flow cytometry, quantitative real-time PCR, total proteome analysis, and multiplex immunoassay.
Data analysis revealed the up-regulation of Il 6 gene in the microcirculation of high-salt-fed rats, accompanied by an increased serum level of TNF-alpha cytokine. The high-salt diet resulted in increased proportion of serum mono-unsaturated fatty acids and saturated fatty acids, reduced levels of linoleic (C18:2 ω-6) and α-linolenic (C18:3 ω-3) acid, and increased levels of palmitoleic acid (C16:1 ω-7). The high-salt diet had distinct, lymphoid compartment-specific effects on leukocyte subpopulations, which could be attributed to the increased expression of salt-sensitive SGK-1 kinase. Complete proteome analysis revealed high-salt-diet-induced vascular tissue remodeling and perturbations in energy metabolism. Interestingly, many of the observed effects were reversed by ANGII supplementation.
Low-grade systemic inflammation induced by a HSD could be related to suppressed ANGII levels. The effects of HSD involved changes in Th17 and Treg cell distribution, vascular wall remodeling, and a shift in lipid and arachidonic acid metabolism.
背景/目的：不受限制地增加食盐（NaCl）摄入与氧化应激和炎症有关，导致内皮功能障碍和动脉粥样硬化。然而，关于盐负荷早期盐诱导免疫调节作用的数据很少。
本研究采用短期盐负荷动物模型，包括雄性 Sprague Dawley 大鼠在 7 天内分别摄入高盐饮食（HSD；4%NaCl）或标准实验室饲料（低盐；LSD；0.4%NaCl）。通过向一组高盐饮食大鼠中添加血管紧张素 II（ANGII）输注来测试 ANGII 抑制的贡献。处理外周血/肠系膜淋巴结白细胞、脑血管和血清样本，用于流式细胞术、定量实时 PCR、全蛋白质组分析和多重免疫分析。
数据分析显示，高盐喂养大鼠微循环中 Il 6 基因上调，伴随 TNF-α细胞因子血清水平升高。高盐饮食导致血清单不饱和脂肪酸和饱和脂肪酸比例增加，亚油酸（C18:2 ω-6）和α-亚麻酸（C18:3 ω-3）水平降低，棕榈油酸（C16:1 ω-7）水平升高。高盐饮食对淋巴细胞区室的白细胞亚群有明显的、特异性的影响，这可归因于盐敏感的 SGK-1 激酶表达增加。完整蛋白质组分析显示，高盐饮食引起血管组织重塑和能量代谢紊乱。有趣的是，许多观察到的影响可被 ANGII 补充所逆转。
HSD 诱导的低度全身炎症可能与 ANGII 水平降低有关。HSD 的作用涉及 Th17 和 Treg 细胞分布、血管壁重塑以及脂质和花生四烯酸代谢的变化。
