Lipid Research Group, School of Medical Sciences, UNSW Sydney, Sydney, New South Wales, Australia.
Division of Immunology and Inflammation, Imperial College London, London, UK.
J Clin Lipidol. 2019 Sep-Oct;13(5):812-820. doi: 10.1016/j.jacl.2019.07.003. Epub 2019 Jul 15.
Previous studies have demonstrated that elevated cholesterol results in increased white blood cell counts in mouse models. However, there is insufficient evidence to support this in humans.
The objective of the study was to investigate the relationship of plasma lipids with white blood cell counts (basophils, eosinophils, monocytes, neutrophils and lymphocytes) in the Multi-Ethnic Study of Atherosclerosis.
The analysis included 2873 Multi-Ethnic Study of Atherosclerosis participants with a complete white blood count and differential analysis. The cross-sectional association of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride levels with different white blood cell counts was analyzed by multivariable linear regression.
After adjusting for sociodemographic and confounding factors including red blood cell counts, platelet counts, use of lipid-lowering medication, cardiovascular disease risk factors and other lipid measures, and multiple testing correction, a one-standard deviation increment in total cholesterol and low-density lipoprotein cholesterol was associated with 2.8% and 2.3% lower total white blood cell counts, 3.7% and 3.0% lower monocyte counts, and 3.4% and 2.7% lower neutrophil counts (all P < .01). The same increment in logarithm-transformed triglyceride levels was associated with 2.3% higher total white blood cell counts and 4.5% higher lymphocyte counts (both P < .001). Similar results were obtained after excluding participants taking lipid-lowering medication. A one-standard deviation increase in high-density lipoprotein cholesterol was associated with a 1.5% lower white blood cell count (P = .018) but was not significantly associated with changes in any individual cell type.
While significant associations were observed between plasma lipid levels and white blood cell populations, the heterogeneous and modest nature of these relationships makes it hard to support the hypothesis that lipids are in the causal pathway for leukogenesis in humans.
先前的研究表明,胆固醇升高会导致小鼠模型中白细胞计数增加。然而,目前尚无充分证据支持这一观点在人类中存在。
本研究旨在探讨多发性动脉粥样硬化症研究中的血脂与白细胞计数(嗜碱性粒细胞、嗜酸性粒细胞、单核细胞、中性粒细胞和淋巴细胞)之间的关系。
该分析纳入了 2873 名多发性动脉粥样硬化症研究参与者,他们的白细胞计数和分类分析完整。采用多元线性回归分析总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇和甘油三酯水平与不同白细胞计数的横断面关联。
在校正了社会人口统计学和混杂因素(包括红细胞计数、血小板计数、降脂药物使用、心血管疾病危险因素和其他血脂指标)以及多重检验校正后,总胆固醇和低密度脂蛋白胆固醇每增加一个标准差,总白细胞计数分别降低 2.8%和 2.3%,单核细胞计数分别降低 3.7%和 3.0%,中性粒细胞计数分别降低 3.4%和 2.7%(均 P <.01)。对数转化甘油三酯水平每增加一个标准差,总白细胞计数增加 2.3%,淋巴细胞计数增加 4.5%(均 P <.001)。排除服用降脂药物的参与者后,得到了类似的结果。高密度脂蛋白胆固醇每增加一个标准差,白细胞计数降低 1.5%(P =.018),但与任何单个细胞类型的变化均无显著相关性。
虽然观察到血浆脂质水平与白细胞群体之间存在显著关联,但这些关联的异质性和适度性质使得难以支持脂质在人类白细胞生成中的因果途径的假说。