Exploring the complexity of host–pathogen communication is vital to understand why microbes persist within a host, while others are cleared. Here, we employed a dual-sequencing approach to unravel conversational turn-taking of dynamic host–pathogen communications. We demonstrate that upon hitting a host cell, motile Pseudomonas aeruginosa induce a specific gene expression program. This results in the expression of spermidine on the surface, which specifically activates the PIP3-pathway to induce phagocytic uptake into primary or immortalized murine cells. Non-motile bacteria are more immunogenic due to a lower expression of arnT upon host-cell contact, but do not produce spermidine and are phagocytosed less. We demonstrate that not only the presence of pathogen inherent molecular patterns induces immune responses, but that bacterial motility is linked to a host-cell-induced expression of additional immune modulators. Our results emphasize on the value of integrating microbiological and immunological findings to unravel complex and dynamic host–pathogen interactions.

中文翻译：

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活动铜绿假单胞菌中宿主诱导的亚精胺产生触发吞噬细胞的摄取

探索宿主与病原体通讯的复杂性对于理解为什么微生物在宿主体内持续存在而其他微生物被清除至关重要。在这里，我们采用了双测序方法来阐明动态宿主-病原体通信的对话轮流。我们证明，在击中宿主细胞后，活动的铜绿假单胞菌会诱导特定的基因表达程序。这导致亚精胺在表面表达，特异性激活 PIP3 途径，诱导原代或永生化小鼠细胞的吞噬摄取。非运动细菌由于宿主细胞接触时 arnT 表达较低而具有更强的免疫原性，但不产生亚精胺并且被吞噬较少。我们证明，不仅病原体固有分子模式的存在会诱导免疫反应，而且细菌的运动性也与宿主细胞诱导的其他免疫调节剂的表达有关。我们的结果强调了整合微生物学和免疫学发现来揭示复杂和动态的宿主-病原体相互作用的价值。