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Involvement of lipid microdomains in human endothelial cells infected by Streptococcus agalactiae type III belonging to the hypervirulent ST-17
Memórias do Instituto Oswaldo Cruz ( IF 2.8 ) Pub Date : 2020-03-16 , DOI: 10.1590/0074-02760190398
Beatriz Jandre Ferreira 1 , Pamella Silva Lannes-Costa 1 , Gabriela da Silva Santos 1 , Cláudia Mermelstein 2 , Marcelo Einicker-Lamas 2 , Prescilla Emy Nagao 1
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BACKGROUND Streptococcus agalactiae capsular type III strains are a leading cause of invasive neonatal infections. Many pathogens have developed mechanisms to escape from host defense response using the host membrane microdomain machinery. Lipid rafts play an important role in a variety of cellular functions and the benefit provided by interaction with lipid rafts can vary from one pathogen to another. OBJECTIVES This study aims to evaluate the involvement of membrane microdomains during infection of human endothelial cell by S. agalactiae. METHODS The effects of cholesterol depletion and PI3K/AKT signaling pathway activation during S. agalactiae-human umbilical vein endothelial cells (HUVEC) interaction were analysed by pre-treatment with methyl-β-cyclodextrin (MβCD) or LY294002 inhibitors, immunofluorescence and immunoblot analysis. The involvement of lipid rafts was analysed by colocalisation of bacteria with flotillin-1 and caveolin-1 using fluorescence confocal microscopy. FINDINGS In this work, we demonstrated the importance of the integrity of lipid rafts microdomains and activation of PI3K/Akt pathway during invasion of S. agalactiae strain to HUVEC cells. Our results suggest the involvement of flotillin-1 and caveolin-1 during the invasion of S. agalactiae strain in HUVEC cells. CONCLUSIONS The collection of our results suggests that lipid microdomain affects the interaction of S. agalactiae type III belonging to the hypervirulent ST-17 with HUVEC cells through PI3K/Akt signaling pathway.

中文翻译:

脂微结构域参与人链球菌无糖链球菌III型感染的内皮细胞,属于超毒性ST-17

背景技术无乳链球菌荚膜III型菌株是侵入性新生儿感染的主要原因。许多病原体已经开发出利用宿主膜微区机制逃避宿主防御反应的机制。脂筏在多种细胞功能中起着重要作用,与脂筏相互作用所提供的益处可能因一种病原体而异。目的本研究旨在评估无乳链球菌感染人内皮细胞过程中膜微区的参与。方法采用甲基-β-环糊精(MβCD)或LY294002抑制剂预处理,免疫荧光和免疫印迹分析法分析无乳链球菌-人脐静脉内皮细胞(HUVEC)相互作用过程中胆固醇的消耗和PI3K / AKT信号通路活化的影响。使用荧光共聚焦显微镜通过将细菌与flotillin-1和Caveolin-1共定位来分析脂质筏的参与。结果在这项工作中,我们证明了无脂链球菌菌株侵染HUVEC细胞过程中脂质筏微区完整性和PI3K / Akt途径活化的重要性。我们的研究结果表明,在HUVEC细胞中无乳链球菌菌株入侵过程中,弗洛蒂林1和小窝蛋白1参与其中。结论我们的结果的收集表明脂质微结构域通过PI3K / Akt信号传导途径影响属于高毒力ST-17的无乳链球菌III型与HUVEC细胞的相互作用。我们证明了无脂链球菌菌株侵染HUVEC细胞过程中脂质筏微区完整性和PI3K / Akt通路活化的重要性。我们的研究结果表明,在HUVEC细胞中无乳链球菌菌株入侵过程中,弗洛蒂林1和小窝蛋白1参与其中。结论我们的结果的收集表明脂质微结构域通过PI3K / Akt信号传导途径影响属于高毒力ST-17的无乳链球菌III型与HUVEC细胞的相互作用。我们证明了无脂链球菌菌株侵染HUVEC细胞过程中脂质筏微区完整性和PI3K / Akt通路活化的重要性。我们的研究结果表明,在HUVEC细胞中无乳链球菌菌株入侵过程中,弗洛蒂林1和小窝蛋白1参与其中。结论我们的结果的收集表明脂质微结构域通过PI3K / Akt信号传导途径影响属于高毒力ST-17的无乳链球菌III型与HUVEC细胞的相互作用。
更新日期:2020-03-16
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