Abstract
Lysophosphatidylcholines are a group of bioactive lipids heavily investigated in the context of inflammation and atherosclerosis development. While present in plasma during physiological conditions, their concentration can drastically increase in certain inflammatory states. Lysophosphatidylcholines are widely regarded as potent pro-inflammatory and deleterious mediators, but an increasing number of more recent studies show multiple beneficial properties under various pathological conditions. Many of the discrepancies in the published studies are due to the investigation of different species or mixtures of lysophatidylcholines and the use of supra-physiological concentrations in the absence of serum or other carrier proteins. Furthermore, interpretation of the results is complicated by the rapid metabolism of lysophosphatidylcholine (LPC) in cells and tissues to pro-inflammatory lysophosphatidic acid. Interestingly, most of the recent studies, in contrast to older studies, found lower LPC plasma levels associated with unfavorable disease outcomes. Being the most abundant lysophospholipid in plasma, it is of utmost importance to understand its physiological functions and shed light on the discordant literature connected to its research. LPCs should be recognized as important homeostatic mediators involved in all stages of vascular inflammation. In this review, we want to point out potential pro- and anti-inflammatory activities of lysophospholipids in the vascular system and highlight recent discoveries about the effect of lysophosphatidylcholines on immune cells at the endothelial vascular interface. We will also look at their potential clinical application as biomarkers.
Highlights
Known as lysolecithins, elevated plasma levels of lysophosphatidylcholines (LPCs) were discovered in the 1950s in certain pathological conditions and were identified as a metabolic product of snake venom [1,2]
Research into bioactive LPCs often resulted in contradicting data, even from experiments performed in the same disease model or cell type
Plasma levels of secretory phospholipases A2 (sPLA2)-IIa correlate with cardiovascular risk and it is, thought to be involved in the pathogenesis of atherosclerosis [158,159,160,161,162]
Summary
Known as lysolecithins, elevated plasma levels of lysophosphatidylcholines (LPCs) were discovered in the 1950s in certain pathological conditions and were identified as a metabolic product of snake venom [1,2]. Inflammation, cell damage and other pathophysiological conditions can profoundly alter the ratio of free to albumin bound LPC through increased production of LPC or decreased plasma levels of albumin [23,24,25]. Plasma LPCs are bioactive lipid metabolites of phosphatidylcholine, which are mainly produced by the action of secretory phospholipases A2 (sPLA2) after removal of a fatty acid [26]. One of the most well studied sPLA2 cleavage product beside LPC is arachidonic acid, which can be further converted via enzymatic (cyclooxygenase-I,-II and lipoxygenase) or non-enzymatic (auto-oxidation with reactive oxygen species) metabolism into prostaglandins, lipoxins and resolvins [33]. Decreased levels of LPC were observed in rheumatoid arthritis [34], diabetes [35], schizophrenia [36], polycystic ovary syndrome [37,38], Alzheimer disease [39,40], pulmonary arterial hypertension [41], aging [42], asthma [43] and liver cirrhosis, where they were associated with increased mortality risk [44]
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