Mounting scientific evidence over decades has established that atherosclerosis is a chronic inflammatory disorder. Among the potentially critical sources of vascular inflammation during atherosclerosis are the components of pathogenic bacteria, especially lipopolysaccharide (LPS). Toll-like receptor (TLR)-4, expressed on different inflammatory cells involved with the recognition of bacterial LPS, has been recognized to have mutations that are prevalent in a number of ethnic groups. Such mutations have been associated with a decreased risk of atherosclerosis. In addition, epidemiological investigations have proposed that LPS confers a risk factor for the development of atherosclerosis. Gram-negative bacteria are the major source of LPS in an individual's serum, which may be generated during subclinical infections. The major cell receptors on inflammatory cells involved in the pathogenesis of atherosclerosis, like macrophages, monocytes, and dendritic cells (DCs), are CD14, MD-2, and LPS binding protein (LBP). These receptors have been blamed for the development of atherosclerosis through dysregulated activation following LPS recognition. Lipoproteins may also play a role in modulating the LPS-induced inflammatory events during atherosclerosis development. In this review article, we attempt to clarify the role of LPS in the initiation and progression of atherosclerotic lesion development.

数十年来越来越多的科学证据表明，动脉粥样硬化是一种慢性炎症性疾病。动脉粥样硬化期间血管炎症的潜在关键来源是致病菌的成分，尤其是脂多糖 (LPS)。Toll 样受体 (TLR)-4，表达于不同的炎症细胞涉及细菌 LPS 的识别，已被认为具有在许多种族中普遍存在的突变。这种突变与动脉粥样硬化风险降低有关。此外，流行病学调查表明，LPS 是动脉粥样硬化发展的危险因素。革兰氏阴性菌是个体血清中 LPS 的主要来源，可能在亚临床感染期间产生。炎症细胞上的主要细胞受体参与动脉粥样硬化的发病机制，如巨噬细胞、单核细胞和树突状细胞 (DC)，是 CD14、MD-2 和 LPS 结合蛋白 (LBP)。这些受体被归咎于 LPS 识别后通过失调的激活而导致动脉粥样硬化的发展。脂蛋白也可能在调节动脉粥样硬化发展过程中 LPS 诱导的炎症事件中发挥作用。在这篇综述文章中，我们试图阐明 LPS 在动脉粥样硬化病变发展的启动和进展中的作用。