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A Highlights from MBoC Selection: Matrix stiffness modulates infection of endothelial cells by Listeria monocytogenes via expression of cell surface vimentin

机译:MBoC选择的亮点:基质刚度通过细胞表面波形蛋白的表达调节单核细胞增生性李斯特菌对内皮细胞的感染

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摘要

Extracellular matrix stiffness (ECM) is one of the many mechanical forces acting on mammalian adherent cells and an important determinant of cellular function. While the effect of ECM stiffness on many aspects of cellular behavior has been studied previously, how ECM stiffness might mediate susceptibility of host cells to infection by bacterial pathogens is hitherto unexplored. To address this open question, we manufactured hydrogels of varying physiologically relevant stiffness and seeded human microvascular endothelial cells (HMEC-1) on them. We then infected HMEC-1 with the bacterial pathogen Listeria monocytogenes (Lm) and found that adhesion of Lm to host cells increases monotonically with increasing matrix stiffness, an effect that requires the activity of focal adhesion kinase (FAK). We identified cell surface vimentin as a candidate surface receptor mediating stiffness-dependent adhesion of Lm to HMEC-1 and found that bacterial infection of these host cells is decreased when the amount of surface vimentin is reduced. Our results provide the first evidence that ECM stiffness can mediate the susceptibility of mammalian host cells to infection by a bacterial pathogen.
机译:细胞外基质硬度(ECM)是作用于哺乳动物贴壁细胞的众多机械力之一,是细胞功能的重要决定因素。虽然先前已经研究了ECM刚度对细胞行为的许多方面的影响,但迄今为止,还没有探索ECM刚度如何介导宿主细胞对细菌病原体感染的敏感性。为了解决这个悬而未决的问题,我们制造了具有不同生理相关硬度的水凝胶,并在其上植入了人类微血管内皮细胞(HMEC-1)。然后,我们用细菌病原体单核细胞增生性李斯特菌(Lm)感染HMEC-1,发现Lm对宿主细胞的粘附随着基质刚度的增加而单调增加,这种作用需要粘着斑激酶(FAK)的活性。我们将细胞表面波形蛋白鉴定为介导Lm对HMEC-1的硬度依赖性粘附的候选表面受体,并发现当表面波形蛋白的量减少时,这些宿主细胞的细菌感染也会减少。我们的结果提供了第一个证据,表明ECM刚度可以介导哺乳动物宿主细胞对细菌病原体感染的敏感性。

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