Kadl Alexandra, Bochkov Valery N, Huber Joakim, Leitinger Norbert
Department of Vascular Biology and Thrombosis Research, Medical University of Vienna, Vienna, Austria.
Antioxid Redox Signal. 2004 Apr;6(2):311-20. doi: 10.1089/152308604322899378.
Acute inflammation is characterized by an accumulation of polymorphonuclear cells (PMNs), generation of reactive oxygen species, subsequent apoptosis of PMNs, and finally phagocytosis of apoptotic cells by macrophages. Recently, it has been demonstrated that during apoptosis oxidation of membrane phospholipids, especially phosphatidylserine, occurs. Moreover, we have shown that membrane vesicles released from apoptotic cells contain biologically active oxidized phospholipids. The involvement of oxidized phospholipids in the development of atherosclerosis, which is described as a chronic inflammatory disease, is increasingly recognized. These oxidized phospholipids were shown to induce several proinflammatory genes, such as monocyte chemoattractant protein 1 or interleukin-8, and it is hypothesized that lipid oxidation products also play a role in other chronic inflammatory disorders. On the other hand, oxidized phospholipids were shown to exert antiendotoxin effects by inhibiting lipopolysaccharide-induced signaling, representing a possible feedback loop during gram-negative infection. Additionally, it has been described that oxidized phospholipids are capable of inducing genes such as heme oxygenase-1 that are important for the resolution of acute inflammation. Moreover, oxidized phospholipids serve as recognition signals on apoptotic cells facilitating phagocytosis. In this review, we discuss the hypothesis that oxidized phospholipids generated in apoptotic cells (a) propagate chronic inflammation and (b) contribute to the resolution of acute inflammation.
急性炎症的特征是多形核细胞（PMNs）积聚、活性氧的产生、随后PMNs的凋亡，以及最终巨噬细胞对凋亡细胞的吞噬作用。最近，已经证明在凋亡过程中会发生膜磷脂尤其是磷脂酰丝氨酸的氧化。此外，我们已经表明，凋亡细胞释放的膜囊泡含有具有生物活性的氧化磷脂。氧化磷脂在动脉粥样硬化（一种被描述为慢性炎症性疾病）发展中的作用越来越受到认可。这些氧化磷脂被证明可诱导几种促炎基因，如单核细胞趋化蛋白1或白细胞介素-8，并且据推测脂质氧化产物在其他慢性炎症性疾病中也起作用。另一方面，氧化磷脂被证明通过抑制脂多糖诱导的信号传导发挥抗内毒素作用，这代表革兰氏阴性感染期间可能的反馈回路。此外，已经描述氧化磷脂能够诱导对急性炎症消退很重要的基因，如血红素加氧酶-1。此外，氧化磷脂作为凋亡细胞上的识别信号促进吞噬作用。在这篇综述中，我们讨论了凋亡细胞中产生的氧化磷脂（a）传播慢性炎症和（b）促进急性炎症消退的假说。
