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Alcoholic liver disease remains one of the most common causes of chronic liver disease in the world. The severity of liver damage related to alcohol varies among different individuals and even within any given individual at different times. Certain symptoms, signs, and abnormal findings on laboratory tests help clinicians distinguish among the various stages of alcohol-induced liver damage and, thus,...
Kupffer cells play a major role in alcoholic liver disease. Oxidative stress and endotoxin are major mediators of the inflammatory process in alcoholic hepatitis. Recent evidence supports the suggestion that endotoxin-induced signal transduction begins with CD14-mediated activation of Toll-receptor 4 and subsequent activation of nuclear factor-kappa B (NF-κB) binding activity. Free radicals from reduced...
The role that inflammatory cell injury plays in the pathogenesis of alcoholic liver disease is reviewed with emphasis on granulocytes and immunocytes. New insights regarding the mechanism of lymphocytic migration from the portal vein and lymphocytic-mediated hepatocellular injury are also reviewed.
The presence of polymorphonuclear leukocytes (neutrophils) in liver parenchyma is a prominent feature of alcoholic hepatitis. However, the pathophysiological importance of these phagocytes and potential injury mechanisms in alcoholic hepatitis remain unclear. This review summarizes the current knowledge on basic mechanisms of neutrophil-induced liver injury as it emerged from studying a number of...
Activated monocytes and macrophages have been postulated to play an important role in the pathogenesis of alcoholic liver disease (ALD). Monocyte activation can be documented by measurement of neopterin, adhesion cell molecules, and certain proinflammatory cytokines and chemokines. We first became interested in the role of monocytes and monocyte-derived cytokines in ALD in relation to altered zinc...
Alcohol drinking and viral hepatitis are both recognized as major causes of liver disease worldwide, and they frequently coexist and synergistically cause liver injury in patients with chronic liver disease. Several mechanisms have been implicated in exacerbation of liver injury in patients with alcohol drinking and viral hepatitis. These include impairment of host defense and liver regeneration by...
Both clinical findings and results of experiments with animal models of alcoholic hepatitis have shown the importance of cytokine-mediated cell-cell interactions in the onset of ethanol-induced liver damage. Proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1beta (IL-1β), and interleukin-6, are released from Kupffer cells or infiltrating neutrophils and macrophages...
The pathogenesis of alcohol-related liver disease (ALD) remains inadequately explained. Increasing alcohol intake is associated with an increased risk of ALD, but many heavy drinkers develop no liver damage. An explanation for ALD susceptibility requires theories that extend beyond a biochemical understanding of alcohol metabolism. Several hepatic cell populations are involved in the pathogenesis...
The cause of alcoholic liver disease (ALD) is multifactorial and poorly understood. It is clear that alcohol alone is not responsible for most of the changes associated with ALD and that cofactors are involved in initiation and production of ALD. One cofactor that has received a great deal of attention recently is the concomitant infection with hepatitis C virus (HCV) and alcohol abuse. The interactive...
Leukocyte infiltration in the liver is one of the most important features of alcoholic liver disease. However, in alcoholic hepatitis, the role of polymorphonuclear neutrophils (PMNs) in liver injury still remains to be fully elucidated. Furthermore, the migration of PMNs and their presence in the liver during alcoholic hepatitis have not been fully investigated. Up-regulation of chemokine secretion...
The normal liver contains a large number of lymphocytes, which include not only specialized natural killer (NK) and NKT cells but also CD4 and CD8 T cells. Whereas some of these cells are terminally differentiated effector cells that are destined to die by apoptosis, many of them are not and include immunocompetent cells that traffic through the liver to provide continuing immune surveillance as well...
The National Institute on Alcohol Abuse and Alcoholism and the Office of Rare Diseases, National Institutes of Health, sponsored a satellite symposium on ''Cellular and Molecular Mechanisms of Alcoholic Hepatitis'' at the 24th Annual Scientific Meeting of the Research Society on Alcoholism, Montreal, Quebec, Canada, June 2001. Alcohol intake is a major cause of hepatitis that may lead to alcoholic...
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