Inhibitory Effects of Escherichia coli on the Formation and Development of Staphylococcus epidermidis Biofilm.

In the present study, we examined whether a commensal gut bacterium Escherichia coli might prevent the formation and development of the biofilm of Staphylococcus epidermidis, a nosocomial extraintestinal pathogen but not a gut microorganism. When co-cultured with S. epidermidis, E. coli strain ATCC 35218, a non-pathogenic strain, was found to be dominant in the biofilm formed on the surface of wells of a microtiter plate. In addition, E. coli significantly incorporated and grew in a niche preoccupied by S. epidermidis biofilm. Two other E. coli strains (strain K-12 and B) also showed to interfere the biofilm formation by S. epidermidis. In contrast, S. epidermidis could not grow in a niche preoccupied by E. coli biofilm. These results suggest that, through inhibition of the formation and development of the biofilm, E. coli may eliminate S. epidermidis from the gastrointestinal tract.

Interaction of Escherichia coli and its culture supernatant with Vibrio vulnificus during biofilm formation.

Vibrio vulnificus is a foodborne pathogen causing septicemia with high mortality rate. In this study, we explored how Escherichia coli, one of the commensal bacteria in the human gastrointestinal tract, can interact with V. vulnificus. Our study results show that the amount of biofilm produced by V. vulnificus was reduced in the presence of E. coli ATCC 35218, although the growth of V. vulnificus L-180 remained unaffected. We also detected an antibiofilm effect of E. coli culture supernatant against V. vulnificus, which could not be reduced even after heat treatment. These findings indicate that E. coli and its culture supernatant may be suitable to prevent biofilm formation by V. vulnificus. By contrast, live cells of V. vulnificus could reduce the amount of preformed E. coli biofilm, but its culture supernatant could not. This suggests that the cell-associated factors contribute toward reduction in E. coli biofilm. Therefore, we speculate that ingestion of an infectious dose of V. vulnificus might induce dislodging of the commensal bacteria from the intestinal epithelia and thus can colonize to initiate the infection.