库普弗电池
促炎细胞因子
肝硬化
肝损伤
酒精性肝病
炎症
脂多糖
TLR4型
肿瘤坏死因子α
脂肪变性
酒精性肝炎
纤维化
化学
生物
免疫学
内分泌学
医学
病理
内科学
作者
Megan R. McMullen,Michele T. Pritchard,Laura E. Nagy
标识
DOI:10.1007/978-1-59745-242-7_15
摘要
Chronic consumption of ethanol induces hepatic steatosis and inflammation, which can eventually lead to more severe liver injury, characterized by fibrosis and cirrhosis. Recruitment of neutrophils to the liver, as well as activation of Kupffer cells, mediates the inflammatory responses observed after chronic ethanol exposure. Kupffer cells, the resident macrophages of the liver, are critical to the onset of ethanol-induced liver injury. Activation of Kupffer cells leads to an increased production of proinflammatory cytokines, such as tumor necrosis factor-alpha and also reactive oxygen species, a process mediated in part by changes in lipopolysaccharide-induced TLR4-dependent signal transduction. The isolation and culture of Kupffer cells is an important technique with which one can elucidate the mechanisms that contribute to alcoholic liver injury.
科研通智能强力驱动
Strongly Powered by AbleSci AI