McClain Craig J, Song Zhenyuan, Barve Shirish S, Hill Daniell B, Deaciuc Ion
Department of Internal Medicine, University of Louisville Medical Center, Louisville, Kentucky 40292, USA.
Am J Physiol Gastrointest Liver Physiol. 2004 Sep;287(3):G497-502. doi: 10.1152/ajpgi.00171.2004.
Alcoholic liver disease (ALD) remains a leading cause of death from liver disease in the United States for which there is no FDA-approved therapy. Abnormal cytokine metabolism is a major feature of ALD. Elevated serum concentration levels of TNF-alpha and TNF-alpha-inducible cytokines/chemokines, such as IL-6, -8, and -18, have been reported in patients with alcoholic hepatitis and/or cirrhosis, and levels correlated with markers of the acute phase response, liver function, and clinical outcome. Studies in animal models support an etiologic role for cytokines in the liver injury of ALD. Cytokines, such as transforming growth factor-beta, play a critical role in the fibrosis of ALD. Multiple new strategies are under investigation to modulate cytokine metabolism as a form of therapy for ALD.
酒精性肝病(ALD)仍是美国肝病致死的主要原因,目前尚无美国食品药品监督管理局(FDA)批准的治疗方法。细胞因子代谢异常是ALD的一个主要特征。据报道,酒精性肝炎和/或肝硬化患者血清中肿瘤坏死因子-α(TNF-α)以及TNF-α诱导的细胞因子/趋化因子(如白细胞介素-6、-8和-18)的浓度水平升高,且这些水平与急性期反应标志物、肝功能及临床结局相关。动物模型研究支持细胞因子在ALD肝损伤中起病因学作用。细胞因子,如转化生长因子-β,在ALD的纤维化过程中起关键作用。目前正在研究多种新策略来调节细胞因子代谢,以此作为ALD的一种治疗方式。