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Toll样受体4在幽门螺旋杆菌感染致动脉粥样硬化中的作用 被引量:6

The Role of Toll-like Receptor 4 in Atherosclerosis Induced by Helicobacter Pylori Infection
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摘要 动脉粥样硬化(As)是一种慢性炎症反应性疾病,幽门螺旋杆菌(Hp)感染与As性疾病的相关性研究日益引起关注,其促进As进展的具体机制尚未完全阐明。Toll样受体4(TLR4)是天然免疫反应的重要受体,在微生物致病因子及其产物引起宿主主动和被动免疫中有重要作用,参与动脉硬化的发生和发展。TLR4在As形成的多种细胞均有表达。TLR4通过捕获Hp的致病因子脂多糖后启动细胞内信号途径,进而引起核因子κB依赖的转录,引起一系列细胞因子及化学因子的释放,增强炎症反应而致病。本文就Hp、TLR4信号通路及其在As中的作用作一综述,为As疾病的防治提供新思路。 Atherosclerosis( As) is a chronic inflammatory and immune disease. The correlation between Helicobacter pylori( Hp) infection and atherosclerotic disease has received increasing attention. However,the clear mechanism of Hp contributing to the development of As has not been completely elucidated. Toll-like receptor 4( TLR4) is an important pattern recognition receptor,which induces innate immunity and induction of acquired immunity by microorganism.TLR4 plays a pivotal role in the initiation and progression of atherosclerosis. TLR4 is expressed on many cells involved in the formation of As. By means of capturing lipopolysaccharide from Hp,TLR4 initiates intracellular signal pathway and leads nuclear factor-kappa B transcription and many inflammatory factors release,and results in inflammatory injury. This article makes a summary on Hp,TLR4 signal pathway and its effects on the pathogenesis of atherosclerosis,and provides an implication for prevention and treatment of atherosclerotic artery diseases.
出处 《中国动脉硬化杂志》 CAS 北大核心 2015年第8期855-858,共4页 Chinese Journal of Arteriosclerosis
关键词 动脉粥样硬化 幽门螺旋杆菌 TOLL样受体4 Atherosclerosis Helicobacter Pylori Toll-like Receptor 4
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  • 1Wolf D, Stachon P, Bode C, et al. Inflammatory mecha-nisms in atherosclerosis [ J ]. Hamostaseologie, 2014, 34 (1) : 63-71.
  • 2Charakida M, Tousoulis D. Infections and atheromatous plaque : current therapeutic implications [ J ]. Curt Pharm Des, 2013, 19(9) : 1 638-650.
  • 3Rosenfeld ME, Campbell LA. Pathogens and atherosclerosis: update on the potential contribution of multiple infec- tious organisms to the pathogenesis of atherosclerosis [ J ]. Thromb Haemost, 2011, 106(5): 858-867.
  • 4Izadi M, Fazel M, Sharubandi SH, et al. Helicobacter species in the atherosclerotic plaques of patients with coro- nary artery disease[ J]. Cardiovasc Pathol, 2012, 21(4) : 307-311.
  • 5Lu Z, Li Y, Jin J, et al. Toll-like receptor 4 activation in microvascular endothelial cells triggers a robust inflammatory response and cross talk with mononuclear cells via interleukin-6[ J]. Arterioseler Thromb Vase Biol, 2012, 32 (7) : 1 696-706.
  • 6Marshall B J, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration [ J ]. Lancet, 1984, 1(8390) : 1 311-315.
  • 7Innocenti M, Svennerholm AM, Quiding-Jarbrink M. Heli- eobacter pylori lipopolysaceharides preferentially induce CXC chemokine production in human monocytes [ J ]. Infect Immun, 2001, 69(6) : 3 800-808.
  • 8Kowalski M, Pawlik M, Konturek JW, et al. Helicobacter pylori infection in coronary artery disease [ J ]. J Physiol Pharmacol, 2006, 57 (Suppl 3) : 101-111.
  • 9Budzynski J, Kozinski M, K/opocka M, et al. Clinical significance of Helicobaeter pylori infection in patients with a- cute coronary syndromes: an overview of current evidence [ J ]. Clin Res Cardiol, 2014, 103 ( 11 ) : 855-856.
  • 10Blum A, Tamir S, Mualem K, et al. Endothelial dysfunction is reversible in Helicobacter pylori-positive subjects [J]. Am J Med, 2011, 124(12) : 1 171-174.

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