This Article Full Text Full Text (PDF) Other Versions of this Article: IAI.00096-08v1 76/6/2531    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Google Scholar Articles by Jones, S. A. Articles by Conway, T. PubMed PubMed Citation Articles by Jones, S. A. Articles by Conway, T.

 Previous Article  |  Next Article 

Infection and Immunity, June 2008, p. 2531-2540, Vol. 76, No. 6
0019-9567/08/$08.00+0     doi:10.1128/IAI.00096-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Glycogen and Maltose Utilization by Escherichia coli O157:H7 in the Mouse Intestine

Advanced Center for Genome Technology, University of Oklahoma, Norman, Oklahoma 73019,¹ Statens Serum Institute, 2300 Copenhagen S, Denmark,² Department of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island 02881³

Received 23 January 2008/ Returned for modification 23 February 2008/ Accepted 7 March 2008

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.

Published ahead of print on 17 March 2008.

Editor: A. J. Bäumler