Cholesterol, inflammation and innate immunity.
Cholesterol, inflammation and innate immunity.
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DOI：
10.1038/nri3793
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发表时间：
2015-02
期刊：
影响因子：
--
通讯作者：
Yvan-Charvet L
中科院分区：
文献类型：
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作者：
Tall AR;Yvan-Charvet L
高胆固醇血症导致巨噬细胞和其他免疫细胞中的胆固醇积累，这促进炎症反应，包括Toll样受体（TLR）信号传导的增强、炎性小体活化以及骨髓和脾脏中单核细胞和中性粒细胞的产生。在细胞水平上，TLR信号传导的激活导致胆固醇流出减少，这导致胆固醇进一步积累和炎症反应的放大。虽然通过促进炎症反应的胆固醇积累可能在对感染的反应中具有有益的作用，但它会导致与慢性代谢性炎症相关的疾病，包括动脉粥样硬化和肥胖症。治疗性干预，如增加高密度脂蛋白的产生或输注，可能会切断胆固醇积累和炎症之间的联系，并对代谢性疾病患者产生有益的影响。
Hypercholesterolaemia leads to cholesterol accumulation in macrophages and other immune cells, which promotes inflammatory responses, including augmentation of Toll-like receptor (TLR) signalling, inflammasome activation, and the production of monocytes and neutrophils in the bone marrow and spleen. On a cellular level, activation of TLR signalling leads to decreased cholesterol efflux, which results in further cholesterol accumulation and the amplification of inflammatory responses. Although cholesterol accumulation through the promotion of inflammatory responses probably has beneficial effects in the response to infections, it worsens diseases that are associated with chronic metabolic inflammation, including atherosclerosis and obesity. Therapeutic interventions such as increased production or infusion of high-density lipoproteins may sever the links between cholesterol accumulation and inflammation, and have beneficial effects in patients with metabolic diseases.