Comparison of carbon nutrition for pathogenic and commensal Escherichia coli strains in the mouse intestine.

Citation data:

Infection and immunity, ISSN: 1098-5522, Vol: 76, Issue: 3, Page: 1143-52

Publication Year:
Usage 99
Abstract Views 95
Downloads 2
Link-outs 2
Captures 204
Readers 199
Exports-Saves 5
Mentions 1
Blog Mentions 1
Citations 159
Citation Indexes 159
Repository URL:;
Fabich, Andrew J.; Jones, Shari A.; Chowdhury, Fatema Z.; Cernosek, Amanda; Anderson, April; Smalley, Darren; McHargue, J. Wesley; Hightower, G. Aaron; Smith, Joel T.; Autieri, Steven M.; Leatham, Mary P.; Lins, Jeremy J.; Allen, Regina L.; Laux, David C.; Cohen, Paul S.; Conway, Tyrrell Show More Hide
American Society for Microbiology; DigitalCommons@URI
Immunology and Microbiology
Most Recent Blog Mention
article description
The carbon sources that support the growth of pathogenic Escherichia coli O157:H7 in the mammalian intestine have not previously been investigated. In vivo, the pathogenic E. coli EDL933 grows primarily as single cells dispersed within the mucus layer that overlies the mouse cecal epithelium. We therefore compared the pathogenic strain and the commensal E. coli strain MG1655 modes of metabolism in vitro, using a mixture of the sugars known to be present in cecal mucus, and found that the two strains used the 13 sugars in a similar order and cometabolized as many as 9 sugars at a time. We conducted systematic mutation analyses of E. coli EDL933 and E. coli MG1655 by using lesions in the pathways used for catabolism of 13 mucus-derived sugars and five other compounds for which the corresponding bacterial gene system was induced in the transcriptome of cells grown on cecal mucus. Each of 18 catabolic mutants in both bacterial genetic backgrounds was fed to streptomycin-treated mice, together with the respective wild-type parent strain, and their colonization was monitored by fecal plate counts. None of the mutations corresponding to the five compounds not found in mucosal polysaccharides resulted in colonization defects. Based on the mutations that caused colonization defects, we determined that both E. coli EDL933 and E. coli MG1655 used arabinose, fucose, and N-acetylglucosamine in the intestine. In addition, E. coli EDL933 used galactose, hexuronates, mannose, and ribose, whereas E. coli MG1655 used gluconate and N-acetylneuraminic acid. The colonization defects of six catabolic lesions were found to be additive with E. coli EDL933 but not with E. coli MG1655. The data indicate that pathogenic E. coli EDL933 uses sugars that are not used by commensal E. coli MG1655 to colonize the mouse intestine. The results suggest a strategy whereby invading pathogens gain advantage by simultaneously consuming several sugars that may be available because they are not consumed by the commensal intestinal microbiota.