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Nat Microbiol. 2018 Feb;3(2):243-252. doi: 10.1038/s41564-017-0065-7. Epub 2017 Nov 27.

Activation of Vibrio cholerae quorum sensing promotes survival of an arthropod host.

Author information

1
Division of Infectious Diseases, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
2
Department of Entomology and Nematology, University of Florida, Gainesville, FL, USA.
3
University of Massachusetts Medical School, Worcester, MA, USA.
4
Department of Biology, AC #2237, Amherst College, Amherst, MA, USA.
5
Division of Signal Transduction/Mass Spectrometry Core, Beth Israel Deaconess Medical Center, Boston, MA, USA.
6
Department of Medicine, Harvard Medical School, Boston, MA, USA.
7
Emerging Pathogens Institute University of Florida, Gainesville, FL, USA.
8
Department of Environmental & Global Health, School of Public Health and Health Profession, University of Florida, Gainesville, FL, USA.
9
Division of Infectious Diseases, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. paula.watnick@childrens.harvard.edu.
10
Department of Microbiology and Immunobiology, Harvard Medical Schoolm, Boston, MA, USA. paula.watnick@childrens.harvard.edu.

Abstract

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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