부산대학교 도서관

ABSTRACTDifferent Escherichia colistrains 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. coliMG1655, E. coliHS, or E. coliNissle 1917) and 10 days later were fed 105CFU 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. colistrains using different nutrients in the intestine. Mice were also precolonized with any of five commensal E. colistrains for 10 days and then were fed 105CFU of E. coliEDL933, an O157:H7 pathogen. E. coliNissle 1917 and E. coliEFC1 limited growth of E. coliEDL933 in the intestine (103to 104CFU/gram of feces), whereas E. coliMG1655, E. coliHS, and E. coliEFC2 allowed growth to higher numbers (106to 107CFU/gram of feces). Importantly, when E. coliEDL933 was fed to mice previously co-colonized with three E. colistrains (MG1655, HS, and Nissle 1917), it was eliminated from the intestine (<10 CFU/gram of feces). These results confirm that commensal E. colistrains can provide a barrier to infection and suggest that it may be possible to construct E. coliprobiotic strains that prevent growth of pathogenic E. colistrains in the intestine.