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KMID : 1235920110030010013
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Medical Journal of Catholoc University of Daegu
2011 Volume.3 No. 1 p.13 ~ p.18
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Pathogenesis of Alcoholic Liver Disease
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Lee Chang-Hyeong
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Abstract
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Alcoholic liver disease remains a major cause of morbidity and mortality worldwide. The development of alcoholic liver disease is a complex process which include oxidative and immunologic damages. Oxidative stress plays an important role in pathogenesis of alcoholic liver injury. The main source of free oxygen species is cytochrome P4502E1 which can be induced by ethanol. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Chronic ethanol consumption contributes to increased gut permeability and increased release of lipopolysaccharide (LPS, endotoxin) from gut lumen into portal circulation. LPS sensitizes Kupffer cells to activation via toll-like receptor 4. This sensitization enhances the production of proinflammatory cytokines and oxygen species that contribute hepatocytes dysfunction, necrosis and apoptosis of hepatocytes. Innate immune responses in Kupffer cells due to gut derived LPS and adaptive immune response against adduct antigens of alcohol and acetaldehyde metabolism are key role in liver damage.
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KEYWORD
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Oxidative stress, Endotoxin, Kupffer cells
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