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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

Comparison of Carbon Nutrition for Pathogenic and Commensal Escherichia coli Strains in the Mouse Intestine

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  • Media type: E-Article
  • Title: Comparison of Carbon Nutrition for Pathogenic and Commensal Escherichia coli Strains in the Mouse Intestine
  • Contributor: 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
  • imprint: American Society for Microbiology, 2008
  • Published in: Infection and Immunity
  • Language: English
  • DOI: 10.1128/iai.01386-07
  • ISSN: 0019-9567; 1098-5522
  • Origination:
  • Footnote:
  • Description: <jats:title>ABSTRACT</jats:title> <jats:p> The carbon sources that support the growth of pathogenic <jats:italic>Escherichia coli</jats:italic> O157:H7 in the mammalian intestine have not previously been investigated. In vivo, the pathogenic <jats:italic>E. coli</jats:italic> 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 <jats:italic>E. coli</jats:italic> 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 <jats:italic>E. coli</jats:italic> EDL933 and <jats:italic>E. coli</jats:italic> 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 <jats:italic>E. coli</jats:italic> EDL933 and <jats:italic>E. coli</jats:italic> MG1655 used arabinose, fucose, and <jats:italic>N</jats:italic> -acetylglucosamine in the intestine. In addition, <jats:italic>E. coli</jats:italic> EDL933 used galactose, hexuronates, mannose, and ribose, whereas <jats:italic>E. coli</jats:italic> MG1655 used gluconate and <jats:italic>N</jats:italic> -acetylneuraminic acid. The colonization defects of six catabolic lesions were found to be additive with <jats:italic>E. coli</jats:italic> EDL933 but not with <jats:italic>E. coli</jats:italic> MG1655. The data indicate that pathogenic <jats:italic>E. coli</jats:italic> EDL933 uses sugars that are not used by commensal <jats:italic>E. coli</jats:italic> 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. </jats:p>
  • Access State: Open Access