摘要
Kupffer细胞(Kupffer cells,KCs)是体内最大的巨噬细胞群,他们参与了肝脏多种疾病的发生发展.体外原代培养是研究KCs生物学功能的重要手段,获得较多数量、较高纯度和活性的KCs是研究其作用机制的首要条件.许多吞噬颗粒和可溶性物质都可以和KCs细胞膜上的受体结合进而激活KCs,其中最重要的是脂多糖(lipopolysaccharide,Kupffer细胞(Kupffer cells,KCs)是体内最大的巨噬细胞群,他们参与了肝脏多种疾病的发生发展.体外原代培养是研究KCs生物学功能的重要手段,获得较多数量、较高纯度和活性的KCs是研究其作用机制的首要条件.许多吞噬颗粒和可溶性物质都可以和KCs细胞膜上的受体结合进而激活KCs,其中最重要的是脂多糖(lipopolysaccharide,LPS).LPS经过Toll样受体4(Toll-like receptor4,TLR4)信号途径直接激活K Cs,导致一系列炎症因子产生增多.高浓度的LPS还可以直接进入细胞内,导致Caspase11途径的激活,促进白介素-1β(interleukin 1 beta,IL-1β)的成熟和释放.KCs在脓毒症、内毒素耐受以及急性胰腺炎中扮演了重要角色,本文将对其在上述疾病中的作用及相关分子机制做一综述.
Kupffer cells(KCs) are also known as liver inherent macrophages,which account for the largest part of human tissue macrophages and participate in the pathogenesis of various liver diseases.In vitro study using primary culture is a valuable tool for the exploration of specific immunological functions of KCs.Obtaining KCs with high purity and activity is the basis for research.A large number of phagocytosable particles and soluble substances can activate KCs by binding to specific receptors on the membrane.The most important molecule that activates KCs is lipopolysaccharide(LPS).A tiny quantity of LPS will drive a Toll-like receptor 4(TLR4)-dependent proinflammatory response that alerts the host to the presence of infection.Higher quantities of LPS,which reach the cytoplasm,will trigger inflammasome activation,interleukin-1beta(IL-1β) production and,ultimately,cell death.KCs play an important role in sepsis,endotoxin tolerance and acute pancreatitis.In this review,we describe the role of KCs in these diseases and the underlying molecular mechanisms.
出处
《世界华人消化杂志》
CAS
2015年第11期1776-1783,共8页
World Chinese Journal of Digestology
基金
国家自然科学基金资助项目
Nos.81301656
81401622~~