{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T11:42:47Z","timestamp":1791200567143,"version":"4.2.0"},"reference-count":22,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[2004,8]]},"abstract":"<jats:p>Ethanol consumption is known to cause significant acute liver damage resulting in hepatic fibrosis and eventual cirrhosis when consumed chronically. The mechanism(s) by which ethanol exerts its damaging effects on the liver are not well understood; however, recent scientific investigation has begun to delineate the earliest events in alcoholic liver disease. From these studies, it is apparent that components of the innate immune system and, in particular, Kupffer cells, play a significant role in this process. It is also becoming clear that other parts of the immune system including T cells may also be responsible for mediating the devastating effects of chronic alcohol consumption on the liver. This review will highlight recent experiments demonstrating a role for the innate immune response in the initiation and progression of alcohol-induced liver hepatitis and subsequent organ damage.<\/jats:p>","DOI":"10.1152\/ajpgi.00094.2004","type":"journal-article","created":{"date-parts":[[2004,7,10]],"date-time":"2004-07-10T01:44:10Z","timestamp":1089423850000},"page":"G310-G314","source":"Crossref","is-referenced-by-count":116,"title":["Recent Advances in Alcoholic Liver Disease III. 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