胆固醇、炎症与固有免疫。
Cholesterol, inflammation and innate immunity.
作者信息
Tall Alan R, Yvan-Charvet Laurent
机构信息
Division of Molecular Medicine, Department of Medicine, Columbia University, 630 West 168th Street, New York, New York 10032, USA.
University of Nice, Unité Mixte de Recherce (UMR), Institut national de la Santé et de la Recherche Médicale U1065, 062104 Nice Cedex 3, France.
出版信息
Nat Rev Immunol. 2015 Feb;15(2):104-16. doi: 10.1038/nri3793.
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.
高胆固醇血症会导致巨噬细胞和其他免疫细胞中胆固醇的积累，从而促进炎症反应，包括Toll样受体（TLR）信号传导增强、炎性小体激活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信号传导的激活会导致胆固醇流出减少，进而导致进一步的胆固醇积累和炎症反应的放大。尽管通过促进炎症反应而导致的胆固醇积累可能在对感染的反应中具有有益作用，但它会使与慢性代谢性炎症相关的疾病恶化，包括动脉粥样硬化和肥胖症。诸如增加高密度脂蛋白的产生或输注等治疗干预措施可能会切断胆固醇积累与炎症之间的联系，并对代谢性疾病患者产生有益影响。
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