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• W2107875458 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." @default.
• W2107875458 created "2016-06-24" @default.
• W2107875458 creator A5011071986 @default.
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• W2107875458 date "2012-05-04" @default.
• W2107875458 modified "2023-10-18" @default.
• W2107875458 title "Oxidized LDLs Inhibit TLR-induced IL-10 Production by Monocytes: A New Aspect of Pathogen-Accelerated Atherosclerosis" @default.
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• W2107875458 doi "https://doi.org/10.1007/s10753-012-9472-3" @default.
• W2107875458 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3397235" @default.
• W2107875458 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22556042" @default.
• W2107875458 hasPublicationYear "2012" @default.
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