Biomechanics of Borrelia burgdorferi Vascular Interactions
Biomechanics of Borrelia burgdorferi Vascular Interactions
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DOI：
10.1016/j.celrep.2016.08.013
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发表时间：
2016-09-06
期刊：
影响因子：
8.8
通讯作者：
Moriarty, Tara J.
中科院分区：
文献类型：
--
作者：
Ebady, Rhodaba;Niddam, Alexandra F.;Moriarty, Tara J.
微生物的全身传播对于许多感染性疾病的进展至关重要，并且与细菌感染引起的大多数死亡率相关。介导关键传播步骤的物理机制，即细菌与血管中血管内皮细胞的结合，仍然未知。在这里，我们表明，莱姆病螺旋体伯氏疏螺旋体在生理剪切应力下的内皮相互作用机制类似于选择素依赖性白细胞滚动。具体地，这些相互作用通过机械负荷沿着一系列粘附复合物的转移来介导，并且通过细菌粘附素BBK 32的系链和捕获键特性来稳定。此外，我们发现，在流动下施加在粘合剂上的力可能足够小，以允许由细菌鞭毛马达驱动的主动迁移。这些发现提供了对细菌-血管相互作用的生物力学的深入了解，并证明传播细菌和循环宿主免疫细胞在生理剪切应力下与内皮细胞相互作用具有广泛保守的机制。
Systemic dissemination of microbes is critical for progression of many infectious diseases and is associated with most mortality due to bacterial infection. The physical mechanisms mediating a key dissemination step, bacterial association with vascular endothelia in blood vessels, remain unknown. Here, we show that endothelial interactions of the Lyme disease spirochete Borrelia burgdorferi under physiological shear stress mechanistically resemble selectin-dependent leukocyte rolling. Specifically, these interactions are mediated by transfer of mechanical load along a series of adhesion complexes and are stabilized by tethers and catch bond properties of the bacterial adhesin BBK32. Furthermore, we found that the forces imposed on adhesive bonds under flow may be small enough to permit active migration driven by bacterial flagellar motors. These findings provide insight into the biomechanics of bacterial-vascular interactions and demonstrate that disseminating bacteria and circulating host immune cells share widely conserved mechanisms for interacting with endothelia under physiological shear stress.