Oxidized LDLs inhibit TLR-induced IL-10 production by monocytes: a new aspect of pathogen-accelerated atherosclerosis.
Oxidized LDLs inhibit TLR-induced IL-10 production by monocytes: a new aspect of pathogen-accelerated atherosclerosis.
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DOI：
10.1007/s10753-012-9472-3
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发表时间：
2012-08
期刊：
影响因子：
5.1
通讯作者：
Pryjma, Juliusz
中科院分区：
文献类型：
--
作者：
Bzowska, Malgorzata;Nogiec, Anna;Skrzeczynska-Moncznik, Joanna;Mickowska, Barbara;Guzik, Krzysztof;Pryjma, Juliusz
人们普遍认为，氧化低密度脂蛋白和局部感染或循环中的内毒素参与了动脉粥样硬化各个阶段的慢性炎症过程。动脉粥样硬化病变的标志细胞--单核细胞和巨噬细胞--能够检测和整合来自脂蛋白和病原体的复杂信号，并对一系列免疫调节细胞因子做出反应。在这项研究中，我们展示了oxLDLS对单核细胞应答TLR2和TLR4配体产生抗炎白介素10的强烈抑制作用。相比之下，在牙龈卟啉单胞菌(一种与动脉粥样硬化相关的口腔病原体)的脂多糖刺激下，促炎性肿瘤坏死因子的分泌甚至略有增加。OxLDLS的调节活性可能是通过改变对病原体相关分子模式的识别来解释的，这种模式涉及血清蛋白，特别是Vitronectin。我们还提出了Vitronectin受体、CD11b和TLR2之间的相互作用。目前的数据支持病原体加速动脉粥样硬化的新途径，该途径依赖于氧化型低密度脂蛋白介导的对TLR配体的抗炎反应的调节。本文的在线版本(doi：10.1007/s10753-0129472-3)包含补充材料，授权用户可以使用。
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. The online version of this article (doi:10.1007/s10753-012-9472-3) contains supplementary material, which is available to authorized users.
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影响因子：
37.8
作者：
Desvarieux, M;Demmer, RT;Papapanou, PN
通讯作者：
Papapanou, PN
DOI：
10.1161/01.atv.0000078603.90302.4a
发表时间：
2003-07-01
影响因子：
8.7
作者：
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通讯作者：
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作者：
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作者：
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通讯作者：
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影响因子：
5.4
作者：
HUANG, SA;ENDO, RI;NEMEROW, GR
通讯作者：
NEMEROW, GR