Abstract
BackgroundThe ability of a bacterial strain to competitively exclude or displace other strains can be attributed to the production of narrow spectrum antimicrobials, the bacteriocins. In an attempt to evaluate the importance of bacteriocin production for Escherichia coli strain residence in the gastrointestinal tract, a murine model experimental evolution study was undertaken.ResultsSix colicin-producing, yet otherwise isogenic, E. coli strains were administered and established in the large intestine of streptomycin-treated mice. The strains' persistence, population density, and doubling time were monitored over a period of 112 days. Early in the experiment only minor differences in population density between the various colicin-producing and the non-producing control strains were detected. However, over time, the density of the control strains plummeted, while that of the colicin-producing strains remained significantly higher (F(7,66) = 2.317; P < 0.0008).ConclusionThe data presented here support prior claims that bacteriocin production may play a significant role in the colonization of E. coli in the gastrointestinal tract. Further, this study suggests that the ability to produce bacteriocins may prove to be a critical factor in determining the success of establishing probiotic E. coli in the gastrointestinal tract of humans and animals.
Highlights
The ability of a bacterial strain to competitively exclude or displace other strains can be attributed to the production of narrow spectrum antimicrobials, the bacteriocins
This study was designed to examine the colonization and persistence of colicinogenic E. coli strains in the mouse GI tract following a single administration
Mice treated with streptomycin to eradicate their resident enterobacterial flora were inoculated with streptomycin resistant bacteriocin producing strains that were monitored for 112 days by weekly sampling of mouse pellets
Summary
The ability of a bacterial strain to competitively exclude or displace other strains can be attributed to the production of narrow spectrum antimicrobials, the bacteriocins. A dominant, resident strain will normally persist in the GI tract for periods of months to years, until it is eventually replaced by one of the many transient strains continually passing through the intestinal lumen. The basis for these periodic shifts is not known and has recently become the focus of a large body of research [2]. In part, this increased interest in the dynamics of E. coli strains is due to dysbiosis, or microbial imbalances of the normal human microflora of the GI tract. This common outcome of antibiotic therapies is considered to be a contributing factor to many chronic and degenerative dis-
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