Department of Internal Medicine 3 - Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Department of Internal Medicine 2 - Cardiology and Angiology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.
Atherosclerosis. 2020 Oct;311:67-72. doi: 10.1016/j.atherosclerosis.2020.08.030. Epub 2020 Sep 8.
Oxidation of low-density lipoprotein (LDL) and oxidized LDL-mediated activation of the innate immune system have been recognized as early key events during the pathogenesis of atherosclerosis. Recent evidence identified eosinophils as a major source of enzymatic lipid oxidation and suggested a potential role of type 2 immunity in atherogenesis. However, the involvement of individual type 2 immune cell subsets involved in this process has been incompletely defined. We therefore sought to determine the role of eosinophils during LDL oxidation and the pathogenesis of this disease.
Using eosinophil-deficient dblGATA1 mice, we studied the role of eosinophils in two established mouse models of atherosclerosis.
These experiments revealed that the presence of eosinophils did neither affect biomarkers of LDL oxidation nor atherosclerotic lesion development.
The obtained results show that LDL oxidation and development of atherosclerosis are largely independent of eosinophils or eosinophil-mediated LDL oxidation.
氧化型低密度脂蛋白(LDL)和氧化型 LDL 介导的固有免疫系统激活,被认为是动脉粥样硬化发病机制中的早期关键事件。最近的证据将嗜酸性粒细胞确定为酶促脂质氧化的主要来源,并提示 2 型免疫在动脉粥样形成中的潜在作用。然而,涉及该过程的个体 2 型免疫细胞亚群的参与尚未完全确定。因此,我们试图确定嗜酸性粒细胞在 LDL 氧化和该疾病发病机制中的作用。
使用嗜酸性粒细胞缺陷型 dblGATA1 小鼠,我们研究了嗜酸性粒细胞在两种已建立的动脉粥样硬化小鼠模型中的作用。
这些实验表明,嗜酸性粒细胞的存在既不影响 LDL 氧化的生物标志物,也不影响动脉粥样硬化病变的发展。
获得的结果表明,LDL 氧化和动脉粥样硬化的发展在很大程度上独立于嗜酸性粒细胞或嗜酸性粒细胞介导的 LDL 氧化。