乙醇影响LPS易位和播散作用的研究进展

Research Progress of Influence of LPS Translocation and Dissemination by Alcohol

乙醇相关性因素往往与慢性炎症相关。导致此类炎症的主因在于肠道微生物产生的脂多糖（LPS）。乙醇可影响肠道黏膜的完整性和通透性，导致肠道黏膜通透性增高、屏障结构缺损，显著增加LPS从肠道易位的概率。从肠道易位的LPS经胃肠道淋巴管和门静脉进入体循环，经门脉途径大部分LPS可被肝脏解毒，经淋巴途径则可有大量LPS进入体循环，进而导致全身性炎症反应的发生，可引起远端靶器官损害。LPS的播散途径还可以影响释放入循环系统的炎性介质的种类，进而影响个体的炎症反应状态。

Chronic inflammation is commonly associated with alcohol-related medical conditions. The key inducer of such inflammation is gut microflora-derived lipopolysaecharide （LPS）. Alcohol can significantly increase the translocation of LPS from the gut. After passing through the gut epithelium, LPS can enter the systemic circulation by some routes, leading to persistent systemic inflammation and ultimately, to organ damage. This article focuses on the translocation and dissemination of LPS passing through the gut epithelium, and wants to introduce the latest research progress of influence of LPS translocation and dissemination by alcohol.