Advances in alcoholic liver disease

被引:42
作者
Song Z. [1 ]
Joshi-Barve S. [1 ]
Barve S. [1 ]
McClain C.J. [1 ]
机构
[1] Department of Internal Medicine, Univ. of Louisville Medical Center, Louisville, KY 40292
关键词
Liver Injury; NASH; Alcoholic Liver Disease; Alcoholic Hepatitis; Tumor Necrosis Factor Production;
D O I
10.1007/s11894-004-0029-y
中图分类号
学科分类号
摘要
Cytokines are mediators of cellular communication produced by multiple liver cell types. Cytokines can directly induce either necrosis or apoptosis. They can also recruit such cells as neutrophils and lymphocytes, which can mediate liver damage. Increased levels of hepatotoxic cytokines such as tumor necrosis factor-α are documented in alcoholic liver disease (ALD) and nonalcoholic steatohepatitis (NASH) and have been shown to play a mechanistic role in both of these disease processes. Transforming growth factor-β is a profibrotic cytokine that is critical in hepatic fibrosis. Beneficial cytokines, such as interleukin (IL)-10 and -6, also exist. Such beneficial cytokines as adiponectin are made outside the liver and appear to protect against ALD and NASH. This article reviews the relevance of cytokines in human and experimental forms of liver injury, focusing on modulation of cytokines and the use of beneficial cytokines in treatment and prevention of liver injury in ALD, NASH, and hepatitis C. Copyright © 2004 by Current Science Inc.
引用
收藏
页码:71 / 76
页数:5
相关论文
共 47 条
[1]  
McClain C.J., Barve S., Deaciuc I., Et al., Cytokines in alcoholic liver disease, Semin. Liver Dis., 19, pp. 205-219, (1999)
[2]  
Canbay A., Feldstein A.E., Higuchi H., Et al., Kupffer cell engulfment of apoptotic bodies stimulates death ligand and cytokine expression, Hepatology, 38, pp. 1188-1198, (2003)
[3]  
Joshi-Barve S., Barve S.S., Butt W., Et al., Inhibition of proteasome function leads to NF-kappaB-independent IL-8 expression in human hepatocytes, Hepatology, 38, pp. 1178-1187, (2003)
[4]  
Xu A., Wang Y., Keshaw H., Et al., The fat-derived hormone adiponectin alleviates alcoholic and nonalcoholic fatty liver diseases in mice, J. Clin. Invest., 112, pp. 91-100, (2003)
[5]  
Hill D.B., Barve S., Joshi-Barve S., McClain C., Increased monocyte nuclear factor-kappaB activation and tumor necrosis factor production in alcoholic hepatitis, J. Lab. Clin. Med., 135, pp. 387-395, (2000)
[6]  
Hill D.B., Marsano L.S., McClain C.J., Increased plasma interleukin-8 concentrations in alcoholic hepatitis, Hepatology, 18, pp. 576-580, (1993)
[7]  
Hanck C., Manigold T., Bocker U., Et al., Gene expression of interleukin 18 in unstimulated peripheral blood mononuclear cells of patients with alcoholic cirrhosis, Gut, 49, pp. 106-111, (2001)
[8]  
Le Moine O., Marchant A., De Groote D., Et al., Role of defective monocyte interleukin-10 release in tumor necrosis factor-alpha overproduction in alcoholics cirrhosis, Hepatology, 22, pp. 1436-1439, (1995)
[9]  
Crespo J., Cayon A., Fernandez-Gil P., Et al., Gene expression of tumor necrosis factor alpha and TNF-receptors, p55 and p75, in nonalcoholic steatohepatitis patients, Hepatology, 34, pp. 1158-1163, (2001)
[10]  
Kugelmas M., Hill D.B., Vivian B., Et al., Cytokines and NASH: A pilot study of the effects of lifestyle modification and vitamin E, Hepatology, 38, pp. 413-419, (2003)