Navab Mohamad, Anantharamaiah G M, Fogelman Alan M
Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California in Los Angeles, Room 47-123 CHS, 10833 Le Conte Avenue, Los Angeles, CA 90095-1679, USA.
Trends Cardiovasc Med. 2005 May;15(4):158-61. doi: 10.1016/j.tcm.2005.05.008.
High-density lipoprotein (HDL) appears to have evolved as part of the innate immune system, which in part uses an enhanced oxidative state as a nonspecific means of protecting against many pathogens. In the absence of acute or chronic inflammation, HDL is anti-inflammatory in mice, rabbits, and humans. However, with the onset of a systemic inflammatory state such as what occurs in atherosclerosis, HDL becomes pro-inflammatory, enhancing the inflammatory response. The major apolipoprotein of HDL is apoA-I, which may be altered by oxidative processes in patients with atherosclerosis. As a result, HDL from such patients is less efficient in promoting cellular cholesterol efflux. The ability of HDL to inhibit the inflammatory properties of oxidized phospholipids and low-density lipoproteins is also significantly altered. In mice and monkeys, the administration of an apoA-I-mimetic peptide renders pro-inflammatory HDL anti-inflammatory, improves HDL-mediated cellular cholesterol efflux; in mice, it dramatically inhibits atherosclerosis. Understanding the role of HDL in inflammation may lead to new diagnostic and therapeutic approaches to atherosclerosis and other inflammatory conditions.
高密度脂蛋白（HDL）似乎是作为先天免疫系统的一部分而进化的，先天免疫系统部分地利用增强的氧化状态作为抵御多种病原体的非特异性手段。在没有急性或慢性炎症的情况下，HDL在小鼠、兔子和人类中具有抗炎作用。然而，随着全身性炎症状态的出现，如动脉粥样硬化中发生的情况，HDL会变得促炎，增强炎症反应。HDL的主要载脂蛋白是载脂蛋白A-I，在动脉粥样硬化患者中，它可能会被氧化过程改变。因此，这类患者的HDL在促进细胞胆固醇流出方面效率较低。HDL抑制氧化磷脂和低密度脂蛋白炎症特性的能力也会显著改变。在小鼠和猴子中，给予载脂蛋白A-I模拟肽可使促炎的HDL变为抗炎，改善HDL介导的细胞胆固醇流出；在小鼠中，它能显著抑制动脉粥样硬化。了解HDL在炎症中的作用可能会为动脉粥样硬化和其他炎症性疾病带来新的诊断和治疗方法。
