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首页> 外文期刊>Infection and immunity >Two Strikingly Different Signaling Pathways Are Induced by Meningococcal Type IV Pili on Endothelial and Epithelial Cells
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Two Strikingly Different Signaling Pathways Are Induced by Meningococcal Type IV Pili on Endothelial and Epithelial Cells

机译：脑膜炎球菌IV型菌毛在内皮细胞和上皮细胞上诱导了两种截然不同的信号通路

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Following adhesion on brain microvasculature, Neisseria meningitidis is able to cross the blood-brain barrier (BBB) by recruiting the polarity complex and the cell junction proteins, thus allowing the opening of the paracellular route. This feature is the consequence of the activation by the type IV pili of the β2-adrenergic receptor/β-arrestin signaling pathway. Here, we have extended this observation to primary peripheral endothelial cells, and we report that the interaction of N. meningitidis with the epithelium is strikingly different. The recruitment of the junctional components by N. meningitidis is indeed restricted to endothelial cell lines, and no alteration of the cell-cell junctions can be seen in epithelial monolayers following meningococcal type IV pilus-mediated colonization. Consistently, the β2-adrenergic receptor/β-arrestin pathway was not hijacked by bacteria adhering on epithelial cells. In addition, we showed that the consequences of the bacterial signaling on epithelial cells is different from that of endothelial cells, since N. meningitidis-induced signaling which protects the microcolonies from shear stress on endothelial cells is unable to do so on epithelial cells. Finally, we report that the minor pilin PilV, which has been shown to be essential for endothelial cell response, is not a required bacterial determinant to induce an epithelial cell response. These data demonstrate that even though pilus-mediated signaling induces an apparently similar cortical plaque, in epithelial and endothelial cell lineages, the signaling pathways are strikingly different in both models.
机译：在脑微血管上粘附后，脑膜炎奈瑟氏球菌能够通过募集极性复合物和细胞连接蛋白来穿越血脑屏障（BBB），从而允许细胞旁途径的开放。该特征是β2-肾上腺素能受体/β-arrestin信号传导途径被IV型菌毛激活的结果。在这里，我们已经将此观察扩展到初级外周血管内皮细胞，并且我们报道了脑膜炎奈瑟氏球菌与上皮的相互作用显着不同。脑膜炎奈瑟氏球菌对接合成分的募集确实仅限于内皮细胞系，在脑膜炎球菌IV型菌毛介导的定殖后，在上皮单层中未见细胞-细胞接合的改变。一致地，β2-肾上腺素受体/β-arrestin途径并未被粘附在上皮细胞上的细菌所劫持。另外，我们表明细菌信号传导对上皮细胞的后果与内皮细胞的后果不同，因为脑膜炎奈瑟氏球菌诱导的保护微菌落免受内皮细胞剪切应力的信号传导在上皮细胞上无法做到。最后，我们报告说，小毛绒菌素PilV已被证明是内皮细胞反应必不可少的，它不是诱导上皮细胞反应的必需细菌决定因素。这些数据表明，即使菌毛介导的信号传导在上皮和内皮细胞谱系中诱导出明显相似的皮质斑块，但两种模型中的信号传导途径却截然不同。

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