The gastrointestinal tract is a reservoir of opportunistic pathogens or pathobionts, which benefit from dysbiosis to proliferate in fragilised patients. VRE originate from the gastrointestinal tract, where their proliferation precedes dissemination in the bloodstream, and may lead to systemic infection. Understanding the mechanisms responsible for resistance to intestinal colonisation by VRE is essential for infection control. Only few studies have identified commensal bacteria that enhance resistance to colonisation of the microbiota against VRE. We aimed to identify additional commensal bacteria that contribute to the barrier effect to accelerate gut microbiota recovery after dysbiosis and enhance resistance to colonisation against VRE. We performed a longitudinal analysis of the gut microbiota composition and VRE carriage levels during microbiota recovery in mice colonised with VRE after antibiotic-induced dysbiosis. By combining biological data and mathematical modelling, we identified seven molecular species (OTUs) that correlate negatively with VRE carriage. Seven strains representative of these OTUs have been collected and used in consortium (Mix7) in two different mice lines challenged with VRE. We found that Mix7 allows a better gut microbiota recovery and a reduction of VRE carriage. Differences in the effect to Mix7 between mice were observed with responder and non-responder mice. These differences were associated with variation of the composition of the initial microbiota suggesting potential biomarkers to predict response to Mix7. Higher concentration of acetate, propionate, butyrate, iso-butyrate, valerate and iso-valerate in responder compared to non-responder and control mice have also been observed. So far, none of the supernatant of the 7 strains, alone or in combination, inhibits VRE growth in vitro. Furthermore, the Bacteroidota strain is required for Mix7 effect in vivo in the presence of at least one of the 6 other strains. The study of possible interactions between the strains in co-culture is in progress. Interestingly, 3 of the 7 strains are shared between human and mice and 4 have human functional equivalents. This project may ultimately allow to move towards a personalised medicine by targeting patients at risk and susceptible to respond to the supplementation with commensal anti-VRE strains.