scholarly journals Toll-like receptor 4-dependent Kupffer cell activation and liver injury in a novel mouse model of parenteral nutrition and intestinal injury

Hepatology ◽  
2012 ◽  
Vol 55 (5) ◽  
pp. 1518-1528 ◽  
Author(s):  
Karim C. El Kasmi ◽  
Aimee L. Anderson ◽  
Michael W. Devereaux ◽  
Sophie A. Fillon ◽  
J. Kirk Harris ◽  
...  
Keyword(s):  
Liver Injury ◽  
Mouse Model ◽  
Parenteral Nutrition ◽  
Kupffer Cell ◽  
Cell Activation ◽  
Intestinal Injury ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

Lipopolysaccharides in liver injury: molecular mechanisms of Kupffer cell activation

2002 ◽  
Vol 283 (2) ◽  
pp. G256-G265 ◽  
Author(s):  
Grace L. Su
Keyword(s):  
Liver Injury ◽  
Proinflammatory Cytokines ◽  
Kupffer Cells ◽  
Cell Activation ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Toll Like Receptor ◽  
Lipopolysaccharide Binding Protein ◽  
Toll Like Receptor 4 ◽  
Lipopolysaccharide Binding

Endogenous gut-derived bacterial lipopolysaccharides have been implicated as important cofactors in the pathogenesis of liver injury. However, the molecular mechanisms by which lipopolysaccharides exert their effect are not entirely clear. Recent studies have pointed to proinflammatory cytokines such as tumor necrosis factor-α as mediators of hepatocyte injury. Within the liver, Kupffer cells are major sources of proinflammatory cytokines that are produced in response to lipopolysaccharides. This review will focus on three important molecular components of the pathway by which lipopolysaccharides activate Kupffer cells: CD14, Toll-like receptor 4, and lipopolysaccharide binding protein. Within the liver, lipopolysaccharides bind to lipopolysaccharide binding protein, which then facilitates its transfer to membrane CD14 on the surface of Kupffer cells. Signaling of lipopolysaccharide through CD14 is mediated by the downstream receptor Toll-like receptor 4 and results in activation of Kupffer cells. The role played by these molecules in liver injury will be examined.

scholarly journals Phytosterols Promote Liver Injury and Kupffer Cell Activation in Parenteral Nutrition-Associated Liver Disease

2013 ◽  
Vol 5 (206) ◽  
pp. 206ra137-206ra137 ◽  
Author(s):  
K. C. El Kasmi ◽  
A. L. Anderson ◽  
M. W. Devereaux ◽  
P. M. Vue ◽  
W. Zhang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Parenteral Nutrition ◽  
Kupffer Cell ◽  
Cell Activation

scholarly journals Kupffer cell activation by lipopolysaccharide in rats: Role for lipopolysaccharide binding protein and toll-like receptor 4

Hepatology ◽  
2000 ◽  
Vol 31 (4) ◽  
pp. 932-936 ◽  
Author(s):  
Grace L. Su ◽  
Richard D. Klein ◽  
Alireza Aminlari ◽  
Hong Y. Zhang ◽  
Lars Steinstraesser ◽  
...  
Keyword(s):  
Kupffer Cell ◽  
Cell Activation ◽  
Binding Protein ◽  
Toll Like Receptor ◽  
Lipopolysaccharide Binding Protein ◽  
Toll Like Receptor 4 ◽  
Lipopolysaccharide Binding

The effect of Toll-like receptor 4 on β 2 -glycoprotein I-induced B cell activation in mouse model

2016 ◽  
Vol 71 ◽  
pp. 78-86 ◽  
Author(s):  
Si Cheng ◽  
Chao He ◽  
Hong Zhou ◽  
Xiangmin Kong ◽  
Hongxiang Xie ◽  
...  
Keyword(s):  
Mouse Model ◽  
B Cell ◽  
Cell Activation ◽  
B Cell Activation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Glycoprotein I

scholarly journals CD4+CD25+Foxp3+ regulatory T cells regulate immune balance in unexplained recurrent spontaneous abortion via the Toll-like receptor 4/nuclear factor-κB pathway

2020 ◽  
Vol 48 (12) ◽  
pp. 030006052098094
Author(s):  
Shuang Qin ◽  
Li Li ◽  
Jia Liu ◽  
Jinrui Zhang ◽  
Qing Xiao ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Unexplained Recurrent Spontaneous Abortion ◽  
Tlr4 Antagonist

Objective The present study aimed to evaluate the effects of cluster of differentiation (CD)4+CD25+ forkhead box p3 (Foxp3)+ regulatory T cells (Tregs) on unexplained recurrent spontaneous abortion (URSA) and the associated mechanisms. Methods The proportion of CD4+CD25+Foxp3+ Tregs and inflammatory cytokine concentrations in the peripheral blood of women with URSA were measured by flow cytometry and enzyme-linked immunosorbent assay, respectively. CBA/JxDBA/2J mating was used to establish an abortion-prone mouse model and the model mice were treated with the Toll-like receptor 4 (TLR4) antagonist E5564 and the TLR4 agonist lipopolysaccharide. Results The proportion of CD4+CD25+Foxp3+ Tregs was decreased and the inflammatory response was increased in women with URSA. In the abortion-prone mouse model, E5564 significantly increased the proportion of CD4+CD25+Foxp3+ Tregs, decreased the inflammatory response, and increased Foxp3 mRNA and protein expression. Lipopolysaccharide had adverse effects on the abortion-prone model. Conclusions These data suggest that CD4+CD25+Foxp3+ Tregs regulate immune homeostasis in URSA via the TLR4/nuclear factor-κB pathway, and that the TLR4 antagonist E5564 may be a novel and potential drug for treating URSA.

scholarly journals Isolation of an endotoxin-MD-2 complex that produces Toll-like receptor 4-dependent cell activation at picomolar concentrations

2004 ◽  
Vol 101 (12) ◽  
pp. 4186-4191 ◽  
Author(s):  
T. L. Gioannini ◽  
A. Teghanemt ◽  
D. Zhang ◽  
N. P. Coussens ◽  
W. Dockstader ◽  
...  
Keyword(s):  
Cell Activation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Dependent Cell
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