Journal
CELL
Volume 173, Issue 7, Pages 1742-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2018.05.008
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Funding
- James S. McDonnell Postdoctoral Fellowship
- Allen Discovery Center at Stanford on Systems Modeling of Infection
- Stanford Center for Systems Biology under NIH [P50-GM107615]
- NIH-NIDDK [R01-DK085025]
- Discovery Innovation Fund Award
- Stanford ChEM-H seed funding
- NSF Graduate Research Fellowships [DGE-114747]
- NCI grant [K08 CA184420]
- NATIONAL CANCER INSTITUTE [K08CA184420] Funding Source: NIH RePORTER
- NATIONAL HUMAN GENOME RESEARCH INSTITUTE [T32HG000044] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK085025, R01DK101674] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P50GM107615] Funding Source: NIH RePORTER
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Osmotic diarrhea is a prevalent condition in humans caused by food intolerance, malabsorption, and widespread laxative use. Here, we assess the resilience of the gut ecosystem to osmotic perturbation at multiple length and timescales using mice as model hosts. Osmotic stress caused reproducible extinction of highly abundant taxa and expansion of less prevalent members in human and mouse microbiotas. Quantitative imaging revealed decimation of the mucus barrier during osmotic perturbation, followed by recovery. The immune system exhibited temporary changes in cytokine levels and a lasting IgG response against commensal bacteria. Increased osmolality prevented growth of commensal strains in vitro, revealing one mechanism contributing to extinction. Environmental availability of microbiota members mitigated extinction events, demonstrating how species reintroduction can affect community resilience. Our findings (1) demonstrate that even mild osmotic diarrhea can cause lasting changes to the microbiota and host and (2) lay the foundation for interventions that increase system-wide resilience.
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