Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Analysis of the evolutionary adaptation of an AraC-like global regulatory protein in the murine enteric pathogen Citrobacter rodentium

ABSTRACT: An experiment to test the equivalence of the Citrobacter rodentium RegA and E.Coli SMS 3-5 homologue 8 Conditions (4 Genotypes by 2 treatments) in duplicate. Reference design without dye swaps.

ORGANISM(S): Citrobacter rodentium

SUBMITTER: Matthew Wakefield

PROVIDER: E-GEOD-57689 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Evolutionary adaptation of an AraC-like regulatory protein in Citrobacter rodentium and Escherichia species.

Tan Aimee A Petty Nicola K NK Hocking Dianna D Bennett-Wood Vicki V Wakefield Matthew M Praszkier Judyta J Tauschek Marija M Yang Ji J Robins-Browne Roy R

Infection and immunity 20150126 4

The evolution of pathogenic bacteria is a multifaceted and complex process, which is strongly influenced by the horizontal acquisition of genetic elements and their subsequent expression in their new hosts. A well-studied example is the RegA regulon of the enteric pathogen Citrobacter rodentium. The RegA regulatory protein is a member of the AraC/XylS superfamily, which coordinates the expression of a gene repertoire that is necessary for full pathogenicity of this murine pathogen. Upon stimulat ...[more]

PMID: 25624355

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Project description:The gut microbiota plays a crucial role in susceptibility to enteric pathogens, including Citrobacter rodentium, a model extracellular mouse pathogen that colonizes the colonic mucosa. C. rodentium infection outcomes vary between mouse strains, with C57BL/6 and C3H/HeN mice clearing and succumbing to the infection, respectively. Kanamycin (Kan) treatment at the peak of C57BL/6 mouse infection with Kan-resistant C. rodentium resulted in relocalization of the pathogen from the colonic mucosa and cecum to solely the cecal luminal contents; cessation of the Kan treatment resulted in rapid clearance of the pathogen. We now show that in C3H/HeN mice, following Kan-induced displacement of C. rodentium to the cecum, the pathogen stably colonizes the cecal lumens of 65% of the mice in the absence of continued antibiotic treatment, a phenomenon that we term antibiotic-induced bacterial commensalization (AIBC). AIBC C. rodentium was well tolerated by the host, which showed few signs of inflammation; passaged AIBC C. rodentium robustly infected naive C3H/HeN mice, suggesting that the AIBC state is transient and did not select for genetically avirulent C. rodentium mutants. Following withdrawal of antibiotic treatment, 35% of C3H/HeN mice were able to prevent C. rodentium commensalization in the gut lumen. These mice presented a bloom of a commensal species, Citrobacter amalonaticus, which inhibited the growth of C. rodentium in vitro in a contact-dependent manner and the luminal growth of AIBC C. rodentium in vivo. Overall, our data suggest that commensal species can confer colonization resistance to closely related pathogenic species. IMPORTANCE Gut bacterial infections involve three-way interactions between virulence factors, the host immune responses, and the microbiome. While the microbiome erects colonization resistance barriers, pathogens employ virulence factors to overcome them. Treating mice infected with kanamycin-resistant Citrobacter rodentium with kanamycin caused displacement of the pathogen from the colonic mucosa to the cecal lumen. Following withdrawal of the kanamycin treatment, 65% of the mice were persistently colonized by C. rodentium, which seemed to downregulate virulence factor expression. In this model of luminal gut colonization, 35% of mice were refractory to stable C. rodentium colonization, suggesting that their microbiotas were able to confer colonization resistance. We identify a commensal bacterium of the Citrobacter genus, C. amalonaticus, which inhibits C. rodentium growth in vitro and in vivo. These results show that the line separating commensal and pathogenic lifestyles is thin and multifactorial and that commensals may play a major role in combating enteric infection.

Dataset Information

Analysis of the evolutionary adaptation of an AraC-like global regulatory protein in the murine enteric pathogen Citrobacter rodentium

Publications

Evolutionary adaptation of an AraC-like regulatory protein in Citrobacter rodentium and Escherichia species.

Similar Datasets

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