scholarly journals HMGB1 Contributes to the Expression of P-Glycoprotein in Mouse Epileptic Brain through Toll-Like Receptor 4 and Receptor for Advanced Glycation End Products

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0140918 ◽  
Author(s):  
Yan Chen ◽  
Xian-Jing Huang ◽  
Nian Yu ◽  
Yuan Xie ◽  
Kang Zhang ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Toll Like Receptor ◽  
Advanced Glycation ◽  
Toll Like Receptor 4 ◽  
P Glycoprotein ◽  
Glycation End Products ◽  
End Products

scholarly journals Advanced glycation end-products reduce lipopolysaccharide uptake by macrophages

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245957
Author(s):  
Atsuhiro Kitaura ◽  
Takashi Nishinaka ◽  
Shinichi Hamasaki ◽  
Omer Faruk Hatipoglu ◽  
Hidenori Wake ◽  
...  
Keyword(s):  
Immune Response ◽  
Advanced Glycation End Products ◽  
Innate Immune ◽  
Raw264.7 Cells ◽  
Toll Like Receptor ◽  
Advanced Glycation ◽  
Toll Like Receptor 4 ◽  
Inflammatory Reactions ◽  
Glycation End Products ◽  
End Products

Hyperglycaemia provides a suitable environment for infections and the mechanisms of glucose toxicity include the formation of advanced glycation end-products (AGEs), which comprise non-enzymatically glycosylated proteins, lipids, and nucleic acid amino groups. Among AGE-associated phenotypes, glycolaldehyde-derived toxic AGE (AGE-3) is involved in the pathogenesis of diabetic complications. Internalisation of endotoxin by various cell types contributes to innate immune responses against bacterial infection. An endotoxin derived from Gram-negative bacteria, lipopolysaccharide (LPS), was reported to enhance its own uptake by RAW264.7 mouse macrophage-like cells, and an LPS binding protein, CD14, was involved in the LPS uptake. The LPS uptake induced the activation of RAW264.7 leading to the production of chemokine CXC motif ligand (CXCL) 10, which promotes T helper cell type 1 responses. Previously, we reported that AGE-3 was internalised into RAW264.7 cells through scavenger receptor-1 Class A. We hypothesized that AGEs uptake interrupt LPS uptake and impair innate immune response to LPS in RAW264.7 cells. In the present study, we found that AGE-3 attenuated CD14 expression, LPS uptake, and CXCL10 production, which was concentration-dependent, whereas LPS did not affect AGE uptake. AGEs were reported to stimulate the receptor for AGEs and Toll-like receptor 4, which cause inflammatory reactions. We found that inhibitors for RAGE, but not Toll-like receptor 4, restored the AGE-induced suppression of CD14 expression, LPS uptake, and CXCL10 production. These results indicate that the receptor for the AGE-initiated pathway partially impairs the immune response in diabetes patients.

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