Vibrio fischeri-derived outer membrane vesicles trigger host development.
Vibrio fischeri-derived outer membrane vesicles trigger host development.
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DOI：
10.1111/cmi.12525
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发表时间：
2016-04
影响因子：
3.4
通讯作者：
Ruby E
中科院分区：
文献类型：
--
作者：
Aschtgen MS;Wetzel K;Goldman W;McFall-Ngai M;Ruby E
外膜囊泡（OMV）是许多宿主细胞/微生物相互作用的关键要素。以前的研究Euprymna tuberopes和弧菌fischeri之间的共生关系表明，在12小时内的殖民隐窝深处的鱿鱼的光器官，共生体触发不可逆转的程序在主机的组织发展。在这里，我们报告说，OMV产生的V. fischeri是强大的贡献者，这一进程。第一个可检测到的宿主对OMV的反应是称为血细胞的巨噬细胞样细胞向表面上皮组织的运输增加。我们发现，将鱿鱼暴露于其他弧菌物种无法诱导这种贩运;然而，添加高浓度的OMV，它可以扩散到隐窝中。我们还提供了证据表明，气管细胞毒素（TCT）释放的共生体，这可以诱导血细胞运输，是不是OMV货物的一部分，这表明两个不同的机制，以诱导相同的形态发生事件。通过操纵OMV信号传递的时机和定位，我们表明，只有当能够到达并在隐窝中生长的唯一物种费氏弧菌成功建立持续的定殖时，血细胞运输才被完全诱导。此外，我们的数据表明，宿主检测OMV作为一个共生检查点诱导不可逆的形态发生之前。
Outer membrane vesicles (OMV) are critical elements in many host-cell/microbe interactions. Previous studies of the symbiotic association between Euprymna scolopes and Vibrio fischeri had shown that, within 12 h of colonizing crypts deep within the squid’s light organ, the symbionts trigger an irreversible program of tissue development in the host. Here, we report that OMV produced by V. fischeri are powerful contributors to this process. The first detectable host response to the OMV is an increased trafficking of macrophage-like cells called hemocytes into surface epithelial tissues. We showed that exposing the squid to other Vibrio species fails to induce this trafficking; however, addition of a high concentration of their OMV, which can diffuse into the crypts, does. We also provide evidence that tracheal cytotoxin (TCT) release by the symbionts, which can induce hemocyte trafficking, is not part of the OMV cargo, suggesting two distinct mechanisms to induce the same morphogenesis event. By manipulating the timing and localization of OMV signal delivery, we showed that hemocyte trafficking is fully induced only when V. fischeri, the sole species able to reach and grow in the crypts, succeeds in establishing a sustained colonization. Further, our data suggest that the host detection of OMV serves as a symbiotic checkpoint prior to inducing irreversible morphogenesis.