title: Glycogen and maltose utilization by Escherichia coli O157:H7 in the mouse intestine.
abstract: Mutant screens and transcriptome studies led us to consider whether the metabolism of glucose polymers, i.e., maltose, maltodextrin, and glycogen, is important for Escherichia coli colonization of the intestine. By using the streptomycin-treated mouse model, we found that catabolism of the disaccharide maltose provides a competitive advantage in vivo to pathogenic E. coli O157:H7 and commensal E. coli K-12, whereas degradation of exogenous forms of the more complex glucose polymer, maltodextrin, does not. The endogenous glucose polymer, glycogen, appears to play an important role in colonization, since mutants that are unable to synthesize or degrade glycogen have significant colonization defects. In support of the hypothesis that E. coli relies on internal carbon stores to maintain colonization during periods of famine, we found that by providing a constant supply of a readily metabolized sugar, i.e., gluconate, in the animal's drinking water, the competitive disadvantage of E. coli glycogen metabolism mutants is rescued. The results suggest that glycogen storage may be widespread in enteric bacteria because it is necessary for maintaining rapid growth in the intestine, where there is intense competition for resources and occasional famine. An important implication of this study is that the sugars used by E. coli are present in limited quantities in the intestine, making endogenous carbon stores valuable. Thus, there may be merit to combating enteric infections by using probiotics or prebiotics to manipulate the intestinal microbiota in such a way as to limit the availability of sugars preferred by E. coli O157:H7 and perhaps other pathogens.
authors.affiliation: Advanced Center for Genome Technology, University of Oklahoma, Norman, Oklahoma 73019, USA.
authors.forename: Shari A
authors.initials: SA
authors.lastname: Jones
authors.forename: Mathias
authors.initials: M
authors.lastname: Jorgensen
authors.forename: Fatema Z
authors.initials: FZ
authors.lastname: Chowdhury
authors.forename: Rosalie
authors.initials: R
authors.lastname: Rodgers
authors.forename: James
authors.initials: J
authors.lastname: Hartline
authors.forename: Mary P
authors.initials: MP
authors.lastname: Leatham
authors.forename: Carsten
authors.initials: C
authors.lastname: Struve
authors.forename: Karen A
authors.initials: KA
authors.lastname: Krogfelt
authors.forename: Paul S
authors.initials: PS
authors.lastname: Cohen
authors.forename: Tyrrell
authors.initials: T
authors.lastname: Conway
mesh_terms: D000818:Animals; D024881:Drug Resistance, Bacterial; D004927:Escherichia coli Infections / Q000382:microbiology*; D019453:Escherichia coli O157 / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D005942:Gluconates / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D007422:Intestines / Q000382:microbiology*; D008297:Male; D008320:Maltose / Q000378:metabolism*; D051379:Mice; D009154:Mutation; D010641:Phenotype; D011134:Polysaccharides / Q000378:metabolism; D013307:Streptomycin / Q000494:pharmacology; D013997:Time Factors
chemical_list: D005942:Gluconates; D011134:Polysaccharides; D008320:Maltose; C008315:maltodextrin; D006003:Glycogen; C030691:gluconic acid; D013307:Streptomycin