Leitinger Norbert
Department of Vascular Biology and Thrombosis Research, University of Vienna, Vienna, Austria.
Curr Opin Lipidol. 2003 Oct;14(5):421-30. doi: 10.1097/00041433-200310000-00002.
This review will summarize recent evidence demonstrating that biologically active phospholipid oxidation products modulate inflammatory reactions.
Structural identification of new biologically active oxidized phospholipids and the finding that they can also be formed at inflammatory sites other than the atherosclerotic lesion have expanded the potential role of these compounds in inflammation beyond atherogenesis. Various signaling pathways are induced by oxidized phospholipids, leading to the expression of inflammatory genes by mechanisms that differ from those mediated by the classic inflammatory agonists tumor necrosis factor or lipopolysaccharide. Furthermore, oxidized phospholipids can bind to pattern recognition molecules and thus potently influence inflammation and immune responses during host defense.
During inflammatory processes biologically active lipid oxidation products accumulate that modulate the inflammatory process and may determine the fate and outcome of the body's reaction in acute inflammation during host defense. Oxidized phospholipids may induce and propagate chronic inflammatory processes; however, evidence is accumulating that cells and tissues respond towards these oxidatively formed stress signals also by activation of anti-inflammatory, cytoprotective reactions.
本综述将总结近期证据，证明生物活性磷脂氧化产物可调节炎症反应。
新的生物活性氧化磷脂的结构鉴定以及它们也可在动脉粥样硬化病变以外的炎症部位形成这一发现，扩大了这些化合物在炎症中的潜在作用，其作用范围超出了动脉粥样硬化的发生过程。氧化磷脂可诱导多种信号通路，通过与经典炎症激动剂肿瘤坏死因子或脂多糖介导的机制不同的机制，导致炎症基因的表达。此外，氧化磷脂可与模式识别分子结合，从而在宿主防御过程中有力地影响炎症和免疫反应。
在炎症过程中，生物活性脂质氧化产物会积累，它们调节炎症过程，并可能决定宿主防御期间急性炎症中机体反应的命运和结果。氧化磷脂可能诱导并传播慢性炎症过程；然而，越来越多的证据表明，细胞和组织也会通过激活抗炎、细胞保护反应来应对这些氧化形成的应激信号。
