Enterococcal Metabolite Cues Facilitate Interspecies Niche Modulation and Polymicrobial Infection

Area of Science:

• Microbiology
• Infectious Diseases
• Bacterial Pathogenesis

Background:

• Enterococcus faecalis (E. faecalis) frequently participates in polymicrobial infections, particularly in urinary tracts, catheter sites, and surgical wounds.
• The mechanisms governing polymicrobial colonization and pathogenesis, especially in the context of host defenses like iron limitation, are not well understood.
• Understanding bacterial interactions under nutrient-limited conditions is crucial for developing effective treatments against mixed-species infections.

Purpose of the Study:

• To investigate the role of E. faecalis in mixed-species infections, specifically under conditions of restricted iron availability.
• To elucidate the mechanisms by which E. faecalis influences the growth and survival of co-infecting bacteria, such as Escherichia coli (E. coli).

Main Methods:

• Conducted in vitro and in vivo experiments to assess the impact of E. faecalis on E. coli biofilm formation and survival.
• Analyzed the role of L-ornithine export by E. faecalis as a potential mechanism for modulating the microbial environment.
• Investigated the effect of E. faecalis-derived L-ornithine on E. coli's ability to synthesize enterobactin, a key siderophore for iron acquisition.

Main Results:

• E. faecalis significantly enhanced E. coli biofilm growth and survival in both in vitro and in vivo models under iron-limiting conditions.
• The augmentation of E. coli growth was attributed to the export of L-ornithine by E. faecalis.
• L-ornithine facilitated E. coli's biosynthesis of the enterobactin siderophore, enabling growth in iron-restricted environments.

Conclusions:

• E. faecalis actively modulates the local environment during polymicrobial infections by providing growth-promoting metabolites like L-ornithine.
• This metabolic contribution allows co-infecting bacteria, such as E. coli, to overcome host-imposed iron limitation.
• The findings highlight a novel mechanism by which E. faecalis promotes polymicrobial infections by supporting the growth of other pathogens.