Variation in dietary salt intake induces coordinated dynamics of monocyte subsets and monocyte-platelet aggregates in humans: implications in end organ inflammation.
Variation in dietary salt intake induces coordinated dynamics of monocyte subsets and monocyte-platelet aggregates in humans: implications in end organ inflammation.
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DOI：
10.1371/journal.pone.0060332
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Li YM
中科院分区：
文献类型：
--
作者：
Zhou X;Zhang L;Ji WJ;Yuan F;Guo ZZ;Pang B;Luo T;Liu X;Zhang WC;Jiang TM;Zhang Z;Li YM
单核细胞活化和组织浸润与高盐摄入诱导的靶器官炎症定量相关。我们假设高盐刺激会诱导CD 14 ++ CD 16+单核细胞的扩增，这是具有促炎表型的三种单核细胞亚群之一，与人体靶器官炎症相关。在20名健康志愿者中进行了一项饮食干预研究，从3天的常规饮食开始，然后是7天的高盐饮食（≥15 g NaCl/天）和7天的低盐饮食（≤5 g NaCl/天）。流式细胞术检测3种单核细胞亚群（“经典型”CD 14 ++ CD 16-、“中间型”CD 14 ++ CD 16+和“非经典型”CD 14 + CD 16 ++）的数量及其与单核细胞-血小板聚集体（MPA）的相关性。血氧水平依赖性磁共振成像（BOLD-MRI）用于评估肾缺氧。转换为高盐饮食导致CD 14 ++单核细胞活化和CD 14 ++ CD 16+亚群和MPAs的快速扩增，CD 14 ++ CD 16-和CD 14 + CD 16 ++亚群的百分比相互降低。使用纯化的CD 14 ++单核细胞的体外研究显示，细胞外[Na+]升高可通过ROS依赖性方式导致CD 14 ++ CD 16+扩增。此外，高盐摄入与肾髓质进行性缺氧（R2* 信号增加）和尿单核细胞趋化蛋白-1（MCP-1）排泄增加相关，表明CD 14 ++ CD 16+亚群与肾脏炎症之间存在时空相关性。低盐饮食可以完全逆转上述变化，而饮食干预期间血压水平保持不变。目前的研究表明，短期增加饮食中的盐摄入量可以诱导CD 14 ++ CD 16+单核细胞的扩增，以及MPA的升高，这可能是高盐诱导的终末器官炎症和潜在血栓栓塞风险的潜在细胞基础。此外，这一过程似乎与血压水平的变化基本无关。这一发现提供了饮食盐摄入量，先天免疫和终末器官炎症之间的新联系。
Monocyte activation and tissue infiltration are quantitatively associated with high-salt intake induced target organ inflammation. We hypothesized that high-salt challenge would induce the expansion of CD14++CD16+ monocytes, one of the three monocyte subsets with a pro-inflammatory phenotype, that is associated with target organ inflammation in humans. A dietary intervention study was performed in 20 healthy volunteers, starting with a 3-day usual diet and followed with a 7-day high-salt diet (≥15 g NaCl/day), and a 7-day low-salt diet (≤5 g NaCl/day). The amounts of three monocyte subsets (“classical” CD14++CD16-, “intermediate” CD14++CD16+ and “non-classical” CD14+CD16++) and their associations with monocyte-platelet aggregates (MPAs) were measured by flow cytometry. Blood oxygen level-dependent magnetic resonance imaging (BOLD-MRI) was used to evaluate renal hypoxia. Switching to a high-salt diet resulted in CD14++ monocyte activation and a rapid expansion of CD14++CD16+ subset and MPAs, with a reciprocal decrease in the percentages of CD14++CD16- and CD14+CD16++ subsets. In vitro study using purified CD14++ monocytes revealed that elevation in extracellular [Na+] could lead to CD14++CD16+ expansion via a ROS dependent manner. In addition, high-salt intake was associated with progressive hypoxia in the renal medulla (increased R2* signal) and enhanced urinary monocyte chemoattractant protein-1 (MCP-1) excretion, indicating a temporal and spatial correlation between CD14++CD16+ subset and renal inflammation. The above changes could be completely reversed by a low-salt diet, whereas blood pressure levels remained unchanged during dietary intervention. The present work demonstrates that short-term increases in dietary salt intake could induce the expansion of CD14++CD16+ monocytes, as well as an elevation of MPAs, which might be the underlying cellular basis of high-salt induced end organ inflammation and potential thromboembolic risk. In addition, this process seems largely unrelated to changes in blood pressure levels. This finding provides novel links between dietary salt intake, innate immunity and end organ inflammation.
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影响因子：
13.6
作者：
Munshi, Raj;Johnson, Ali;Zager, Richard A.
通讯作者：
Zager, Richard A.
影响因子：
3.7
作者：
Cox N;Pilling D;Gomer RH
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影响因子：
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作者：
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DOI：
10.1152/ajprenal.00222.2006
发表时间：
2007-02-01
影响因子：
4.2
作者：
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Becker, Bryan N.
影响因子：
2.3
作者：
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