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Infection and Immunity, July 2009, p. 2876-2886, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00059-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Precolonized Human Commensal Escherichia coli Strains Serve as a Barrier to E. coli O157:H7 Growth in the Streptomycin-Treated Mouse Intestine{triangledown}

Mary P. Leatham,1 Swati Banerjee,1 Steven M. Autieri,1 Regino Mercado-Lubo,1 Tyrrell Conway,2 and Paul S. Cohen1*

Department of Cell and Molecular Biology, University of Rhode Island, Kingston, Rhode Island 02881,1 Department of Botany and Microbiology, University of Oklahoma, Norman, Oklahoma 730192

Received 16 January 2009/ Returned for modification 25 February 2009/ Accepted 3 April 2009

Different Escherichia coli strains generally have the same metabolic capacity for growth on sugars in vitro, but they appear to use different sugars in the streptomycin-treated mouse intestine (Fabich et al., Infect. Immun. 76:1143-1152, 2008). Here, mice were precolonized with any of three human commensal strains (E. coli MG1655, E. coli HS, or E. coli Nissle 1917) and 10 days later were fed 105 CFU of the same strains. While each precolonized strain nearly eliminated its isogenic strain, confirming that colonization resistance can be modeled in mice, each allowed growth of the other commensal strains to higher numbers, consistent with different commensal E. coli strains using different nutrients in the intestine. Mice were also precolonized with any of five commensal E. coli strains for 10 days and then were fed 105 CFU of E. coli EDL933, an O157:H7 pathogen. E. coli Nissle 1917 and E. coli EFC1 limited growth of E. coli EDL933 in the intestine (103 to 104 CFU/gram of feces), whereas E. coli MG1655, E. coli HS, and E. coli EFC2 allowed growth to higher numbers (106 to 107 CFU/gram of feces). Importantly, when E. coli EDL933 was fed to mice previously co-colonized with three E. coli strains (MG1655, HS, and Nissle 1917), it was eliminated from the intestine (<10 CFU/gram of feces). These results confirm that commensal E. coli strains can provide a barrier to infection and suggest that it may be possible to construct E. coli probiotic strains that prevent growth of pathogenic E. coli strains in the intestine.

* Corresponding author. Mailing address: Department of Cell and Molecular Biology, University of Rhode Island, Kingston, RI 02881. Phone: (401) 874-5920. Fax: (401) 874-2202. E-mail: pco1697u{at}mail.uri.edu

{triangledown} Published ahead of print on 13 April 2009.

Editor: B. A. McCormick

Infection and Immunity, July 2009, p. 2876-2886, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00059-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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