Oxidized LDLs inhibit TLR-induced IL-10 production by monocytes: a new aspect of pathogen-accelerated atherosclerosis.

Inflammation
Małgorzata BzowskaJuliusz Pryjma

Abstract

It is widely accepted that oxidized low-density lipoproteins and local infections or endotoxins in circulation contribute to chronic inflammatory process at all stages of atherosclerosis. The hallmark cells of atherosclerotic lesions-monocytes and macrophages-are able to detect and integrate complex signals derived from lipoproteins and pathogens, and respond with a spectrum of immunoregulatory cytokines. In this study, we show strong inhibitory effect of oxLDLs on anti-inflammatory interleukin-10 production by monocytes responding to TLR2 and TLR4 ligands. In contrast, pro-inflammatory tumor necrosis factor secretion was even slightly increased, when stimulated with lipopolysaccharide from Porphyromonas gingivalis-an oral pathogen associated with atherosclerosis. The oxLDLs modulatory activity may be explained by altered recognition of pathogen-associated molecular patterns, which involves serum proteins, particularly vitronectin. We also suggest an interaction between vitronectin receptor, CD11b, and TLR2. The presented data support a novel pathway for pathogen-accelerated atherosclerosis, which relies on oxidized low-density lipoprotein-mediated modulation of anti-inflammatory response to TLR ligands.

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Citations

Apr 20, 2013·World Journal of Gastroenterology : WJG·Ying-Ju LiJian-Hua Xiao
Oct 22, 2014·Cellular and Molecular Life Sciences : CMLS·Agnieszka PłóciennikowskaKatarzyna Kwiatkowska
Jan 29, 2014·European Journal of Clinical Investigation·Jung-Su ChangHung-Yi Chiou
May 10, 2017·Molecular Aspects of Medicine·Thomas E Van Dyke
Dec 24, 2018·Antioxidants·Ning Hong AwJorming Goh

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Methods Mentioned

BETA
density gradient centrifugation
flow cytometry
electrophoresis
FCS
enzyme-linked immunosorbent assays
ELISA
with

Software Mentioned

FACSDiva
Origin

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