期刊
NATURE MICROBIOLOGY
卷 3, 期 2, 页码 243-252出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41564-017-0065-7
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资金
- National Institutes of Health [R21 AI109436, R01 AI097405]
- NIH [5P30CA006516, 5P01CA120964]
- NATIONAL CANCER INSTITUTE [P30CA006516, P01CA120964] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI112652, R21AI109436, R01AI097405, R01AI071147] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [P40OD018537] Funding Source: NIH RePORTER
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.
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