Microbiota-derived lantibiotic restores resistance against vancomycin-resistant Enterococcus Research Letter


Authors: Kim, S. G.; Becattini, S.; Moody, T. U.; Shliaha, P. V.; Littmann, E. R.; Seok, R.; Gjonbalaj, M.; Eaton, V.; Fontana, E.; Amoretti, L.; Wright, R.; Caballero, S.; Wang, Z. M. X.; Jung, H. J.; Morjaria, S. M.; Leiner, I. M.; Qin, W.; Ramos, R. J. J. F.; Cross, J. R.; Narushima, S.; Honda, K.; Peled, J. U.; Hendrickson, R. C.; Taur, Y.; van den Brink, M. R. M.; Pamer, E. G.
Title: Microbiota-derived lantibiotic restores resistance against vancomycin-resistant Enterococcus
Abstract: Intestinal commensal bacteria can inhibit dense colonization of the gut by vancomycin-resistant Enterococcus faecium (VRE), a leading cause of hospital-acquired infections1,2. A four-strained consortium of commensal bacteria that contains Blautia producta BPSCSK can reverse antibiotic-induced susceptibility to VRE infection3. Here we show that BPSCSK reduces growth of VRE by secreting a lantibiotic that is similar to the nisin-A produced by Lactococcus lactis. Although the growth of VRE is inhibited by BPSCSK and L. lactis in vitro, only BPSCSK colonizes the colon and reduces VRE density in vivo. In comparison to nisin-A, the BPSCSK lantibiotic has reduced activity against intestinal commensal bacteria. In patients at high risk of VRE infection, high abundance of the lantibiotic gene is associated with reduced density of E. faecium. In germ-free mice transplanted with patient-derived faeces, resistance to VRE colonization correlates with abundance of the lantibiotic gene. Lantibiotic-producing commensal strains of the gastrointestinal tract reduce colonization by VRE and represent potential probiotic agents to re-establish resistance to VRE. © 2019, The Author(s), under exclusive licence to Springer Nature Limited.
Keywords: mus; enterococcus; enterococcus faecium; lactococcus lactis
Journal Title: Nature
Volume: 572
Issue: 7771
ISSN: 0028-0836
Publisher: Nature Publishing Group  
Date Published: 2019-08-01
Start Page: 665
End Page: 669
Language: English
DOI: 10.1038/s41586-019-1501-z
PUBMED: 31435014
PROVIDER: scopus
PMCID: PMC6717508
DOI/URL:
Notes: Source: Scopus
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