Abstract

The virulence mechanisms that allow pathogens to colonize the intestine remain unclear. Here, we show that germ-free animals are unable to eradicate Citrobacter rodentium, a model for human infections with attaching and effacing bacteria. Early in infection, virulence genes were expressed and required for pathogen growth in conventionally raised mice but not germ-free mice. Virulence gene expression was down-regulated during the late phase of infection, which led to relocation of the pathogen to the intestinal lumen where it was outcompeted by commensals. The ability of commensals to outcompete C. rodentium was determined, at least in part, by the capacity of the pathogen and commensals to grow on structurally similar carbohydrates. Thus, pathogen colonization is controlled by bacterial virulence and through competition with metabolically related commensals.

Links

Publisher Full Text

Authors

Kamada N, Kim YG, Sham HP, Vallance BA, Puente JL, Martens EC, Núñez G

Institution

Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.

Source

Science (New York, N.Y.) 336:6086 2012 Jun 8 pg 1325-9

MeSH

Animals
Bacterial Load
Bacterial Proteins
Bacteroides
Citrobacter rodentium
Enterobacteriaceae Infections
Escherichia coli
Feces
Gene Expression Regulation, Bacterial
Germ-Free Life
Intestinal Mucosa
Intestines
Metagenome
Mice
Mice, Inbred C57BL
Microbial Interactions
Specific Pathogen-Free Organisms
Virulence Factors

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22582016