Microbiota assembly during infancy is governed by competition between species and by environmental factors, termed habitat filters, that determine the range of successful traits within the microbial community. Once microbiota assembly is complete, the microbial community contributes to niche protection against enteric pathogens, but the underlying mechanisms are incompletely understood.
We show that neonatal chick colonization with Salmonella enterica serovar (S.) 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 suggests 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, phenocopying 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 protection is lost when the ability to respire oxygen under microaerophilic conditions is genetically ablated in E. coli.
These results suggest competition with endogenous Enterobacterales for oxygen, habitat filtering by short-chain fatty acids and a host-derived habitat filter, epithelial hypoxia, contribute to colonization resistance against Salmonella serovars.
Presented at the 7th International Conference on Poultry Intestinal Health, Cartagena, Colombia, 2022. For information on the next edition, click here.