Wang Shuo, Qing Duxin
Department of Gastroenterology, Xiangya Changde Hospital, Changde Hunan 415000.
Department of Gastroenterology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2020 Aug 28;45(8):999-1004. doi: 10.11817/j.issn.1672-7347.2020.190272.
Alcoholic liver disease (ALD) is a chronic liver disease characterized by large accumulation of lipids in the liver, accompanied by inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. In the different stages of ALD, mediators of the immune system, such as cytokines or inflammasomes, are crucially involved. In the ALD disease spectrum, the upregulation of the inflammatory cascade is the main factor in the development of steatohepatitis into severe alcoholic hepatitis. Activation of the inflammatory cascade requires multiple stimuli. Pyroptosis is a new type of programmed cell death that relies on caspase. Inflammasomes play a crucial role in the process of cell death. Cellular infection or cellular stress can activate inflammatory corpuscles, leading to assembly of inflammasome polyprotein complexes, activation of caspase-1 and its downstream substrates pro-IL-1β, pro-IL-18 and gasdermin D activation and maturation, thus participating in the body's immune inflammatory response and induced cell death. In recent years, there is increasing evidence that activation of inflammatory bodies and pyroptosis play a key role in the development of alcoholic liver disease.
酒精性肝病（ALD）是一种慢性肝病，其特征是肝脏中大量脂质堆积，并伴有炎症、纤维化、肝硬化和肝细胞癌。在ALD的不同阶段，免疫系统的介质，如细胞因子或炎性小体，起着至关重要的作用。在酒精性肝病谱中，炎症级联反应的上调是脂肪性肝炎发展为严重酒精性肝炎的主要因素。炎症级联反应的激活需要多种刺激。细胞焦亡是一种依赖半胱天冬酶的新型程序性细胞死亡。炎性小体在细胞死亡过程中起关键作用。细胞感染或细胞应激可激活炎性小体，导致炎性小体多蛋白复合物的组装、半胱天冬酶-1及其下游底物前白细胞介素-1β、前白细胞介素-18的激活以及gasdermin D的激活和成熟，从而参与机体的免疫炎症反应并诱导细胞死亡。近年来，越来越多的证据表明炎性小体的激活和细胞焦亡在酒精性肝病的发展中起关键作用。
