Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 115, Issue 16, Pages E3779-E3787Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1720133115
Keywords
Vibrio cholerae; zebrafish; type VI secretion system; microbiota; peristalsis
Categories
Funding
- National Science Foundation (NSF) [0922951, 1427957, MCB-1149925]
- M. J. Murdock Charitable Trust
- Kavli Microbiome Ideas Challenge
- American Chemical Society
- American Physical Society
- Kavli Foundation
- National Institute of General Medical Sciences [P50GM098911]
- National Institute of Child Health and Human Development [P01HD22486]
- Scialog Program - Research Corporation for Science Advancement
- Gordon and Betty Moore Foundation through
- Georgia Institute of Technology
- Memorial Sloan Kettering Cancer Center by the Gordon and Betty Moore Foundation
- Simons Foundation [509990, 509992]
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P01HD022486] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P50GM098911] Funding Source: NIH RePORTER
- Direct For Biological Sciences [1149925] Funding Source: National Science Foundation
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Host-associated microbiota help defend against bacterial pathogens; however, the mechanisms by which pathogens overcome this defense remain largely unknown. We developed a zebrafish model and used live imaging to directly study how the human pathogen Vibrio cholerae invades the intestine. The gut microbiota of fish monocolonized by symbiotic strain Aeromonas veronii was displaced by V. cholerae expressing its type VI secretion system (T6SS), a syringe-like apparatus that deploys effector proteins into target cells. Surprisingly, displacement was independent of T6SS-mediated killing of A. veronii, driven instead by T6SS-induced enhancement of zebrafish intestinal movements that led to expulsion of the resident microbiota by the host. Deleting an actin cross-linking domain from the T6SS apparatus returned intestinal motility to normal and thwarted expulsion, without weakening V. cholerae's ability to kill A. veronii in vitro. Our finding that bacteria can manipulate host physiology to influence intermicrobial competition has implications for both pathogenesis and microbiome engineering.
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