Invasion of human aortic endothelial cells by oral viridans group streptococci and induction of inflammatory cytokine production
Invasion of human aortic endothelial cells by oral viridans group streptococci and induction of inflammatory cytokine production
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DOI：
10.1111/j.2041-1014.2010.00597.x
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发表时间：
2011-01-01
影响因子：
3.7
通讯作者：
Oho, T.
中科院分区：
文献类型：
--
作者：
Nagata, E.;de Toledo, A.;Oho, T.
草绿色链球菌是口腔生物膜中的主要细菌，在人类动脉粥样硬化斑块中也有发现。动脉粥样硬化涉及持续的炎症反应，据报道涉及由多种病原体引起的慢性感染。本研究的目的是研究口腔草绿色链球菌对人主动脉内皮细胞（HAECs）的侵袭以及随后活的侵袭HAECs产生的细胞因子。使用抗生素保护试验检查HAECs的细菌入侵，并通过共聚焦扫描激光显微镜观察。过氧化氢酶和细胞松弛素D对HAECs侵袭的抑制作用也进行了研究。用酶联免疫吸附测定法测定受侵袭或感染的HAECs细胞因子的产生，并采用实时聚合酶链反应方法评价细胞因子信使RNA的表达。测试的口腔链球菌能够侵入HAEC。随着共培养时间的延长，侵袭性细菌的数量逐渐增加。在一定的共培养期后，一些微生物对HAECs具有细胞毒性。过氧化氢酶和细胞松弛素D可抑制HAECs的侵袭。被变形链球菌Xc、戈登链球菌DL 1（查利斯）、戈登链球菌ATCC 10558和唾液链球菌ATCC 13419侵袭的HAEC比未侵袭的HAEC产生更多的细胞因子（白细胞介素-6、白细胞介素-8、单核细胞趋化蛋白-1）。S. mutans Xc产生的细胞因子最多，且侵袭HAECs细胞因子mRNA表达较未侵袭HAECs显著增加。这些结果表明，口腔链球菌可能参与动脉粥样硬化的发病机制。
P>Oral viridans group streptococci are the major commensal bacteria of the supragingival oral biofilm and have been detected in human atheromatous plaque. Atherosclerosis involves an ongoing inflammatory response, reportedly involving chronic infection caused by multiple pathogens. The aim of this study was to examine the invasion of human aortic endothelial cells (HAECs) by oral viridans group streptococci and the subsequent cytokine production by viable invaded HAECs. The invasion of HAECs by bacteria was examined using antibiotic protection assays and was visualized by confocal scanning laser microscopy. The inhibitory effects of catalase and cytochalasin D on the invasion of HAECs were also examined. The production of cytokines by invaded or infected HAECs was determined using enzyme-linked immunosorbent assays, and a real-time polymerase chain reaction method was used to evaluate the expression of cytokine messenger RNA. The oral streptococci tested were capable of invading HAECs. The number of invasive bacteria increased with the length of the co-culture period. After a certain co-culture period, some organisms were cytotoxic to the HAECs. Catalase and cytochalasin D inhibited the invasion of HAECs by the organism. HAECs invaded by Streptococcus mutans Xc, Streptococcus gordonii DL1 (Challis), Streptococcus gordonii ATCC 10558 and Streptococcus salivarius ATCC 13419 produced more cytokine(s) (interleukin-6, interleukin-8, monocyte chemoattractant protein-1) than non-invaded HAECs. The HAECs invaded by S. mutans Xc produced the largest amounts of cytokines, and the messenger RNA expression of cytokines by invaded HAECs increased markedly compared with that by non-invaded HAECs. These results suggest that oral streptococci may participate in the pathogenesis of atherosclerosis.