Abstract：
To spread within a host, intracellular Burkholderia form actin tails to generate membrane protrusions into neighboring host cells and use type VI secretion system-5 (T6SS-5) to induce cell-cell fusions. Here, we show that B. thailandensis also uses T6SS-5 to lyse protrusions to directly spread from cell to cell. Dynamin-2 recruitment to the membrane near a bacterium was followed by a short burst of T6SS-5 activity. This resulted in the polymerization of the actin of the newly invaded host cell and disruption of the protrusion membrane. Most protrusion lysis events were dependent on dynamin activity, caused no cell-cell fusion, and failed to be recognized by galectin-3. T6SS-5 inactivation decreased protrusion lysis but increased galectin-3, LC3, and LAMP1 accumulation in host cells. Our results indicate that B. thailandensis specifically activates T6SS-5 assembly in membrane protrusions to disrupt host cell membranes and spread without alerting cellular responses, such as autophagy.
摘要：
在宿主内传播，细胞内伯克霍尔德菌形成肌动蛋白尾巴以产生进入相邻宿主细胞的膜突起，并使用VI型分泌系统-5（T6SS-5）诱导细胞-细胞融合。这里,我们显示B.thailandensis还使用T6SS-5溶解突起以直接在细胞之间传播。Dynamin-2募集到细菌附近的膜上，随后是T6SS-5活性的短暂爆发。这导致新入侵的宿主细胞的肌动蛋白的聚合和突起膜的破坏。大多数突起溶解事件依赖于动态蛋白活性，没有引起细胞-细胞融合，并且未能被半乳糖凝集素-3识别。T6SS-5失活减少了突起溶解，但增加了半乳糖凝集素-3，LC3和LAMP1在宿主细胞中的积累。我们的结果表明，B.thailandensis特异性激活膜突起中的T6SS-5组装以破坏宿主细胞膜并传播而不引起细胞反应，比如自噬。
