II. Alcoholic liver injury involves activation of Kupffer cells by endotoxin.

@article{Thurman1998IIAL,
  title={II. Alcoholic liver injury involves activation of Kupffer cells by endotoxin.},
  author={Ronald G. Thurman},
  journal={American journal of physiology. Gastrointestinal and liver physiology},
  year={1998},
  volume={275 4},
  pages={G605-G611}
}
  • R. Thurman
  • Published 1 October 1998
  • Chemistry, Medicine
  • American journal of physiology. Gastrointestinal and liver physiology
It is well known that females show a greater susceptibility to alcohol-induced liver injury than males. Additionally, females who consume alcohol regularly and have been obese for 10 years or more are at greater risk for both hepatitis and cirrhosis. Female rats on an enteral alcohol protocol exhibit injury more quickly than males, with widespread fatty changes over a larger portion of the liver lobule. Levels of plasma endotoxin, intercellular adhesion molecule-1, free radical adducts… 
Increased severity of alcoholic liver injury in female rats: role of oxidative stress, endotoxin, and chemokines.
TLDR
Findings in ethanol-fed rats suggest that increased endotoxemia and lipid peroxidation in females stimulate NF-kappa B activation and chemokine production, enhancing liver injury.
Chronic alcohol intoxication primes Kupffer cells and endothelial cells for enhanced CC-chemokine production and concomitantly suppresses phagocytosis and chemotaxis.
  • A. Bautista
  • Chemistry, Medicine
    Frontiers in bioscience : a journal and virtual library
  • 2002
TLDR
Data demonstrate that prolonged alcohol consumption may compromise the host to hepatitis as a result of increased chemokine production and at the same time may suppress the innate immune function of hepatic non-parenchymal cells.
Exacerbation of alcoholic liver injury by enteral endotoxin in rats
TLDR
Enteral LPS administration potentiates alcoholic liver necrosis, inflammation, and fibrosis despite efficient endotoxin clearance by the liver and mild systemic endotoxemia that occurs episodically following enteral L PS challenge.
Isolation of Kupffer cells from rats fed chronic ethanol.
TLDR
The isolation and culture of Kupffer cells is an important technique with which one can elucidate the mechanisms that contribute to alcoholic liver injury.
Pathogenesis of alcoholic liver disease: newer mechanisms of injury.
  • D. Crabb
  • Biology, Medicine
    The Keio journal of medicine
  • 1999
TLDR
Advances suggest a number of new approaches as therapy for alcoholic liver injury, including stimulation of Kupffer cells by portal vein endotoxin as a cause of release of cytokines and chemokines, hepatocyte hyper-metabolism, and activation of HSC.
Enhancement of allyl alcohol hepatotoxicity by endotoxin requires extrahepatic factors.
TLDR
LPS augments the hepatotoxicity of allyl alcohol through a mechanism involving extrahepatic factors, one of which may be a component of the coagulation cascade.
Pathogenesis of alcoholic hepatitis
TLDR
Alcohol abuse accounts for more than half of the prev-alence of liver fibrosis and cirrhosis in the western world and features several special characteristics, including elevated gut-derived endotoxinplasma levels.
Lipopolysaccharide-mediated signal transduction: Stabilization of TNF-alpha mRNA contributes to increased lipopolysaccharide-stimulated TNF-alpha production by Kupffer cells after chronic ethanol feeding
TLDR
This model proposes that increased exposure of Kupffer cells to LPS during chronic ethanol consumption results in increased production of inflammatory mediators, in particular TNF-alpha and reactive oxygen species, leading to the progression of fatty liver, inflammation and fibrosis, characteristic of ALD.
Effect of chronic ethanol administration on the in vitro production of proinflammatory cytokines by rat Kupffer cells in the presence of apoptotic cells.
TLDR
Chronic ethanol administration results in an enhanced responsiveness of KCs to produce proinflammatory cytokines indicated by the increased production of inflammatory mediators from KCs obtained from ethanol-fed animals.
Involvement of platelet-activating factor in hepatic apoptosis and necrosis in chronic ethanol-fed rats given endotoxin.
TLDR
It is suggested that PAF is an important mediator of hepatic injury in the ethanol/endotoxin model of alcoholic hepatitis.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 60 REFERENCES
Inactivation of Kupffer cells prevents early alcohol‐induced liver injury
TLDR
It is demonstrated that GdCl3 prevents alcohol‐induced liver injury and suggest strongly that Kupffer cells participate in the early phases of the disease process and might represent a new approach to clinical management of alcohol‐ induced liver injury.
Estrogen increases sensitivity of hepatic Kupffer cells to endotoxin.
TLDR
Estrogen treatment in vivo sensitizes Kupffer cells to LPS, leading to increased toxic mediator production by the liver, and estrogen treatment increased LPS binding protein mRNA dramatically in liver in 6-24 h.
Antibiotics prevent liver injury in rats following long-term exposure to ethanol.
TLDR
Intestinal sterilization prevented alcohol-induced liver injury in the rat, supporting the idea that hypermetabolism and consequent hypoxia caused by activation of Kupffer's cells by endotoxin is involved in the mechanism.
Female rats exhibit greater susceptibility to early alcohol-induced liver injury than males.
TLDR
The purpose of this study was to determine if an enteral alcohol delivery model could be used to study susceptibility of females to alcohol-induced liver injury and to account for increased hepatic injury due to ethanol in the female.
Antibodies to tumor necrosis factor alfa attenuate hepatic necrosis and inflammation caused by chronic exposure to ethanol in the rat
TLDR
The hypothesis that TNF‐ α plays an important role in inflammation and necrosis in alcohol‐induced liver injury and that treatment with anti‐TNF‐α antibody may be therapeutically useful in this disease is supported.
Free radical adducts in the bile of rats treated chronically with intragastric alcohol: inhibition by destruction of Kupffer cells.
TLDR
Free radical formation in ethanol-treated rats has been detected for the first time in a model that exhibits injury characteristic of human alcoholic injury, and signal intensity correlates with hepatotoxicity.
The effects of acute and chronic alcoholism on tumor necrosis factor and the inflammatory response.
Ethanol intoxication has been shown to suppress selected functions of the immune system, thereby compromising host defenses against bacterial infections. Because the macrophage secretory protein,
Alcohol causes both tolerance and sensitization of rat Kupffer cells via mechanisms dependent on endotoxin.
TLDR
Kupffer cells isolated from rats early after ethanol exhibited tolerance to LPS, whereas sensitization was observed later, suggesting that both of these phenomena are caused by gut-derived endotoxin and that sensitization in K upffer cells is caused by increases in CD14.
Ethanol and diet-induced alterations in Kupffer cell function.
TLDR
The results suggest that early in chronic alcohol consumption, the immune system may be stimulated by ethanol, and that during studies of ethanol-induced changes in immune system function, close attention must be given to potentially confounding effects of the diet.
Severity of liver injury in experimental alcoholic liver disease. Correlation with plasma endotoxin, prostaglandin E2, leukotriene B4, and thromboxane B2.
TLDR
The study shows the importance of endotoxin in the pathogenesis of experimental alcoholic liver disease and suggests that endotoxin modulates production of eicosanoids that contribute to the severity of liver injury.
...
1
2
3
4
5
...