Abstract
The prevalence of vancomycin resistant enterococcus (VRE) carrier-state has been increasing in patients of intensive care unit and it would be a public health threat. Different research groups conducted decolonizing VRE with probiotic and the results were controversial. Therefore, a systemic approach to search for the probiotic species capable of decolonizing VRE is necessary. Thus, VRE was co-cultured with ten probiotic species. The fluctuations of each bacterial population were analyzed by 16S rRNA sequencing. Microbial network analysis (MNA) was exploited to identify the most critical species in inhibiting the VRE population. The MNA-selected probiotic cocktail was then validated for its efficacy in inhibiting VRE, decolonizing VRE from Caco-2 cells via three approaches: exclusion, competition, and displacement. Finally, the expression of VRE virulence genes after co-incubation with the probiotic cocktail were analyzed with quantitative real-time PCR (qRT-PCR). The MNA-selected probiotic cocktail includes Bacillus coagulans, Lactobacillus rhamnosus GG, Lactobacillus reuteri, and Lactobacillus acidophilus. This probiotic combination significantly reduces the population of co-cultured VRE and prevents VRE from binding to Caco-2 cells by down-regulating several host-adhesion genes of VRE. Our results suggested the potential of this four-strain probiotic cocktail in clinical application for the decolonization of VRE in human gut.
Highlights
Enterococci, which are harmless commensal bacteria in the human gut [1], can cause opportunistic infections in immunocompromised individuals [2]
Ten strains of probiotic bacteria belonging to the genera of Bacillus, Bifidobacterium, Lactobacillus, Lactococcus, Sporolactobacillus, and Streptococcus were included in this study to determine a formula of probiotics to decolonize vancomycin-resistant enterococci (VRE) in the human gut, as follows: Bacillus coagulans, Bifidobacterium bifidum, Bifidobacterium longum subsp. infantis, Lactococcus lactis subsp. lactis, Lactobacillus plantarum subsp. plantarum, Sporolactobacillus inulinus, Streptococcus salivarius subsp. thermophilus, Lactobacillus rhamnosus GG, Lactobacillus reuteri, and Lactobacillus acidophilus
All of the nine virulence genes of vancomycin-resistant E. faecium (VREfm) were significantly downregulated after co-culturing with Caco-2 cells in the presence of the four-strain probiotic mixture. These results suggest that adherence-associated genes that are responsible for different host environments may act differently under a given condition, and their mRNA expressions were suppressed when VREfm interacting with the four-strain probiotic mixture, reducing the adherence of VREfm to Caco-2 cells
Summary
Enterococci, which are harmless commensal bacteria in the human gut [1], can cause opportunistic infections in immunocompromised individuals [2]. Hospital-acquired infections that are caused by antibiotic-resistant Enterococcus species are difficult to treat and they can be life threatening; they have become a major public health concern and increased the economic burden of patients and governments [6,7,8]. In 2017, the WHO regarded vancomycin-resistant enterococci (VRE) as requiring high priority for research and development of new antibiotics, owing to their global prevalence and the aforementioned risks to public health [15]. In addition to being the most relevant to hospital-acquired infections, E. faecalis and E. faecium are the two main reservoirs for vanA, vanB, and vanM, which are the genes contributing to high levels of resistance to vancomycin; they are the main targets of studies focused on VRE. Vancomycin-resistant E. faecalis has been more frequently detected than other Enterococcus species; E. faecium is recently being increasingly detected [16,17]
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