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Retraction of enteropathogenic E. coli type IV pili promotes efficient host cell colonization, effector translocation and tight junction disruption

机译:肠致病性大肠杆菌IV型菌毛的回缩促进有效的宿主细胞定植,效应子易位和紧密连接破坏

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摘要

Type IV pili (Tfp) play a primary role in mediating the adherence of pathogenic bacteria to their hosts. The pilus filament can retract with an immense force. However, the role of this activity in microbial pathogenesis has not been rigorously explored. Experiments performed on volunteers suggested that the retraction capacity of enteropathogenic Escherichia coli (EPEC) Tfp is required for full virulence. Here we review our recent study in which we showed that the retraction capacity of the EPEC Tfp facilitates tight-junction disruption and actin-rich pedestal formation by promoting efficient bacterial protein effector translocation into epithelial host cells. We also present new data using live imaging confocal microscopy suggesting that EPEC adheres to monolayers in microcolonies and that Tfp retraction facilitates significant changes in the microcolony shape, which may be critical for efficient effector delivery. Our studies hence suggest novel insights into the role of pili retraction in EPEC pathogenesis.
机译:IV型菌毛(Tfp)在介导病原菌与其宿主的粘附中起主要作用。纤毛细丝可以用巨大的力缩回。但是,尚未对此活性在微生物发病机理中的作用进行严格研究。在志愿者身上进行的实验表明,充分致病性需要肠道致病性大肠杆菌(EPEC)Tfp的回缩能力。在这里,我们回顾我们最近的研究,其中我们表明,EPEC Tfp的回缩能力通过促进有效的细菌蛋白效应子易位到上皮宿主细胞中,促进了紧密连接的破坏和富含肌动蛋白的基架的形成。我们还提出了使用实时成像共聚焦显微镜的新数据,这表明EPEC粘附在微菌落中的单层细胞,并且Tfp缩回促进了微菌落形状的显着变化,这对于有效的效应子传递可能至关重要。因此,我们的研究提出了关于菌毛缩回在EPEC发病机理中的作用的新颖见解。

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