Journal
CELL HOST & MICROBE
Volume 25, Issue 1, Pages 128-+Publisher
CELL PRESS
DOI: 10.1016/j.chom.2018.12.003
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Funding
- Vaadia-BARD Postdoctoral Fellowship [FI-505-2014]
- California Agricultural Experimental Station
- USDA/NIFA Multistate Research Project [NE1334]
- Public Health Service [AI060555, AI044170, AI096528, AI112445, AI112949]
- USDA/NIFA award [2015-67015-22930]
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Neonates are highly susceptible to infection with enteric pathogens, but the underlying mechanisms are not resolved. We show that neonatal chick colonization with Salmonella enterica serovar Enteritidis requires a virulence-factor-dependent increase in epithelial oxygenation, which drives pathogen expansion by aerobic respiration. Co-infection experiments with an Escherichia coli strain carrying an oxygen-sensitive reporter suggest that S. Enteritidis competes with commensal Enterobacteriaceae for oxygen. A combination of Enterobacteriaceae and spore-forming bacteria, but not colonization with either community alone, confers colonization resistance against S. Enteritidis in neonatal chicks, pheno-copying germ-free mice associated with adult chicken microbiota. Combining spore-forming bacteria with a probiotic E. coli isolate protects germ-free mice from pathogen colonization, but the protection is lost when the ability to respire oxygen under micro-aerophilic conditions is genetically ablated in E. coll. These results suggest that commensal Enterobacteriaceae contribute to colonization resistance by competing with S. Enteritidis for oxygen, a resource critical for pathogen expansion.
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