Iron acquisition pathways and colonization of the inflamed intestine by Salmonella enterica serovar Typhimurium

- Ferric iron uptake via IroN and TonB uptake contributes to fitness of Salmonella typhimurium in the inflamed intestine.
- Ferrous iron uptake via FeoB contributes to Salmonella fitness in the intestine after antibiotic treatment.
- The benefit conferred by FeoB after antibiotic treatment is independent of T3SS-induced intestinal inflammation.
- Disruption of the gut microbiota by antibiotics may alter the availability of ferrous iron to colonizing Salmonella.

Salmonella enterica serotype Typhimurium is able to expand in the lumen of the inflamed intestine through mechanisms that have not been fully resolved. Here we utilized streptomycin-pretreated mice and dextran sodium sulfate (DSS)-treated mice to investigate how pathways for S. Typhimurium iron acquisition contribute to pathogen expansion in the inflamed intestine. Competitive infection with an iron uptake-proficient S. Typhimurium strain and mutant strains lacking tonB feoB, feoB, tonB or iroN in streptomycin pretreated mice demonstrated that ferric iron uptake requiring IroN and TonB conferred a fitness advantage during growth in the inflamed intestine. However, the fitness advantage conferred by ferrous iron uptake mechanisms was independent of inflammation and was only apparent in models where the normal microbiota composition had been disrupted by antibiotic treatment.