Vibrio cholerae colonizes the human terminal ileum to cause cholera, and the arthropod intestine and exoskeleton to persist in the aquatic environment. Attachment to these surfaces is regulated by the bacterial quorum-sensing signal transduction cascade, which allows bacteria to assess the density of microbial neighbours. Intestinal colonization with V. cholerae results in expenditure of host lipid stores in the model arthropod Drosophila melanogaster. Here we report that activation of quorum sensing in the Drosophila intestine retards this process by repressing V. cholerae succinate uptake. Increased host access to intestinal succinate mitigates infection-induced lipid wasting to extend survival of V. cholerae-infected flies. Therefore, quorum sensing promotes a more favourable interaction between V. cholerae and an arthropod host by reducing the nutritional burden of intestinal colonization.

中文翻译：

---

霍乱弧菌群体感应的激活促进了节肢动物宿主的存活。

霍乱弧菌定居在人类末端回肠以引起霍乱，节肢动物的肠道和外骨骼在水生环境中持续存在。这些表面的附着受到细菌群体感应信号转导级联的调节，这使细菌能够评估微生物邻域的密度。霍乱弧菌的肠道定殖导致节肢动物果蝇果蝇模型中宿主脂质存储的消耗。在这里我们报告果蝇肠道中群体感应的激活通过抑制霍乱弧菌琥珀酸的摄取而延迟了这一过程。寄主对肠道琥珀酸酯的访问增加，减轻了感染引起的脂质浪费，从而延长了霍乱弧菌感染的果蝇的生存期。因此，群体感应促进了V之间更有利的交互。