The Role of Kupffer Cells After Major Liver Surgery

2005 ◽  
Vol 29 (1) ◽  
pp. 48-55
Author(s):  
Hubert A. Prins ◽  
Catharina Meijer ◽  
Petra G. Boelens ◽  
Robert J. Nijveldt ◽  
Michiel P. C. Siroen ◽  
...  
Keyword(s):  
Kupffer Cells ◽  
Liver Surgery

The role of Kupffer cells after major liver surgery

2003 ◽  
Vol 22 ◽  
pp. S53
Author(s):  
H.A. Prins ◽  
R. Holtz ◽  
P.G. Boelens ◽  
J. Diks ◽  
R.J. Nijveldt ◽  
...  
Keyword(s):  
Kupffer Cells ◽  
Liver Surgery

The Role of Kupffer Cells After Major Liver Surgery

2005 ◽  
Vol 29 (1) ◽  
pp. 48-55 ◽  
Author(s):  
H. A. Prins ◽  
C. Meijer ◽  
P. G. Boelens ◽  
R. J. Nijveldt ◽  
M. P. C. Siroen ◽  
...  
Keyword(s):  
Kupffer Cells ◽  
Liver Surgery

Role of Kupffer cells in the ethanol-induced oxidative stress in the liver

10.2741/a455 ◽  
1999 ◽  
Vol 4 (4) ◽  
pp. d589-595 ◽  
Author(s):  
Abraham P Bautista
Keyword(s):  
Oxidative Stress ◽  
Kupffer Cells

Role of neutrophils and Kupffer cells in hepatic cells in hepatic infection: Do we have it wrong?

2004 ◽  
Vol 121 (2) ◽  
pp. 333
Author(s):  
D.R. Jeyarajah ◽  
M.L. Kielar ◽  
X. Zhou ◽  
P. Karimi ◽  
N.L. Frantz ◽  
...  
Keyword(s):  
Kupffer Cells ◽  
Hepatic Cells

scholarly journals The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Severe Liver ◽  
Hepatocellular Necrosis

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.

Putative antihyperpyretic factor induced by LPS in spleen of guinea pigs

2005 ◽  
Vol 289 (3) ◽  
pp. R680-R687 ◽  
Author(s):  
Carlos Feleder ◽  
Vit Perlik ◽  
Ying Tang ◽  
Clark M. Blatteis
Keyword(s):  
Kupffer Cells ◽  
Guinea Pigs ◽  
Collateral Circulation ◽  
Splenic Vein ◽  
Inhibitory Factor ◽  
Febrile Response ◽  
Temperature Changes ◽  
The Core ◽  
Temporally Correlated

We reported previously that the onset of LPS-induced fever, irrespective of its route of administration, is temporally correlated with the appearance of LPS in the liver and that splenectomy significantly increases both the febrile response to LPS and the uptake of LPS by Kupffer cells (KC). To further evaluate the role of the spleen in LPS fever production, we ligated the splenic vein and, 7 and 30 days later, monitored the core temperature changes over 6 h after intraperitoneal (ip) injection of LPS (2 μg/kg). Both the febrile response and the uptake of LPS by KC were significantly augmented. Like splenectomy, splenic vein ligation (SVL) increased the febrile response and LPS uptake by KC until the collateral circulation developed, suggesting that the spleen may normally contribute an inhibitory factor that limits KC uptake of LPS and thus affects the febrile response. Subsequently, to verify the presence of this factor, we prepared splenic extracts from guinea pigs pretreated with LPS (8 μg/kg ip) or pyrogen-free saline, homogenized and ultrafiltered them, and injected them intravenously into splenectomized (Splex) guinea pigs pretreated with LPS (8 μg/kg ip). The results confirmed our presumption that the splenic extract from LPS-treated guinea pigs inhibits the exaggerated febrile response and the LPS uptake by the liver of Splex guinea pigs, indicating the presence of a putative splenic inhibitory factor, confirming the participation of the spleen in LPS-induced fever, and suggesting the existence of a novel antihyperpyretic mechanism. Preliminary data indicate that this factor is a lipid.

Role of CT in Two-Stage Liver Surgery

Radiographics ◽  
2022 ◽  
Vol 42 (1) ◽  
pp. 106-124
Author(s):  
Diego M. Haberman ◽  
Oscar C. Andriani ◽  
Nicole L. Segaran ◽  
Mariano M. Volpacchio ◽  
Maria Lucrecia Micheli ◽  
...  
Keyword(s):  
Liver Surgery ◽  
Two Stage

Role of podoplanin and Kupffer cells in liver injury after ischemia–reperfusion in mice

Surgery Today ◽  
2021 ◽  
Author(s):  
Yuuki Nakata ◽  
Hiroshi Kono ◽  
Yoshihiro Akazawa ◽  
Kazuyoshi Hirayama ◽  
Hiroyuki Wakana ◽  
...  
Keyword(s):  
Liver Injury ◽  
Kupffer Cells ◽  
Ischemia Reperfusion

Selective macrophage depletion in the liver does not prevent the development of the sick euthyroid syndrome in the mouse

1996 ◽  
Vol 134 (4) ◽  
pp. 513-518 ◽  
Author(s):  
Anita Boelen ◽  
Marianne C Platvoet-ter Schiphorst ◽  
Nico van Rooijen ◽  
Wilmar M Wiersinga
Keyword(s):  
Kupffer Cells ◽  
Medical Center ◽  
Academic Medical Center ◽  
Thyroid Hormone Metabolism ◽  
Macrophage Depletion ◽  
Liver Macrophages ◽  
Academic Medical ◽  
Selective Depletion ◽  
Sick Euthyroid

Boelen A, Platvoet-ter Schiphorst MC, van Rooijen N, Wiersinga WM. Selective macrophage depletion in the liver does not prevent the development of the sick euthyroid syndrome in the mouse. Eur J Endocrinol 1996;134:513–8. ISSN 0804–4643 A decreased serum triiodothyronine (T3) level is one of the main characteristics of the sick euthyroid syndrome, caused mainly by a decreased 5′-deiodination of thyroxine (T4) in the liver. Cytokines have been implicated in the pathogenesis of the changes in thyroid hormone metabolism during illness. We therefore investigated the role of cytokines produced by the liver macrophages (Kupffer cells) in the development of the sick euthyroid syndrome, which was induced in mice by a single injection of bacterial endotoxin (lipopolysaccharide) or by 24-h starvation. Experiments were carried out with or without previous selective depletion of liver macrophages by intravenous administration of liposome-encapsulated dichloromethylene diphosphonate. Relative to saline-injected pair-fed controls, the administration of lipopolysaccharide caused a decrease of serum T3 and T4 and liver 5′-deiodinase mRNA. Selective depletion of liver macrophages did not affect these changes. Starvation for 24 h decreased serum T3 and T4, associated with a slight decrease of liver 5′-deiodinase mRNA. There were no differences between macrophage-depleted and non-depleted animals in this respect. In summary, selective depletion of liver macrophages did not affect the decrease in serum T3, T4 or liver 5′-deiodinase mRNA induced by lipopolysaccharide or 24-h starvation in mice. We conclude that cytokines produced by Kupffer cells are not involved in the pathogenesis of the sick euthyroid syndrome in this experimental model. A Boelen, Department of Endocrinology, F5-171 Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

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