Journal
CELL
Volume 185, Issue 19, Pages 3617-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2022.08.003
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Funding
- Dean's Postdoctoral Fellowship
- NIH [F32GM143859, DP1 DK113598, P01 HL147823, R01 DK101674, RM1 GM135102, R01 AI147023]
- Human Frontier Science Program award [LT000493/2018-L]
- Astellas Foundation for Research on Metabolic Disorders
- Stanford Microbiome Therapies Initiative
- NSF [EF-2125383]
- Helmsley Charitable Trust
- Bill and Melinda Gates Foundation
- HHMI-Simons Faculty Scholars Award
- Leducq Foundation
- Stanford-Coulter Translational Research Grants Program
- MAC3 Impact Philanthropies
- Allen Discovery Center at Stanford on Systems Modeling of Infection
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Efforts have been made to model the human gut microbiome in mice, leading to insights into host-microbe interactions. In this study, a defined community of 104 bacterial species from the human gut microbiota was constructed and characterized. New species were identified and added to the community, resulting in increased stability and colonization resistance against pathogenic Escherichia coli. This consortium enables a mechanistic investigation of species and genes on microbiome-associated phenotypes.
Efforts to model the human gut microbiome in mice have led to important insights into the mechanisms of host-microbe interactions. However, the model communities studied to date have been defined or complex, but not both, limiting their utility. Here, we construct and characterize in vitro a defined community of 104 bacterial species composed of the most common taxa from the human gut microbiota (hCom1). We then used an iterative experimental process to fill open niches: germ-free mice were colonized with hCom1 and then challenged with a human fecal sample. We identified new species that engrafted following fecal challenge and added them to hCom1, yielding hCom2. In gnotobiotic mice, hCom2 exhibited increased stability to fecal challenge and robust colonization resistance against pathogenic Escherichia coli. Mice colonized by either hCom2 or a human fecal community are phenotypically similar, suggesting that this consortium will enable a mechanistic interrogation of species and genes on microbiome-associated phenotypes.
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