Chun-Yi Wu, Hung-Tse Huang, Yu-Ting Chiang, Kung-Ta Lee
{"title":"Surfactin inhibits enterococcal biofilm formation via interference with pilus and exopolysaccharide biosynthesis.","authors":"Chun-Yi Wu, Hung-Tse Huang, Yu-Ting Chiang, Kung-Ta Lee","doi":"10.1186/s12866-025-03786-y","DOIUrl":null,"url":null,"abstract":"<p><p>Enterococcus faecalis is a significant pathogen in healthcare settings and is frequently resistant to multiple antibiotics. This resistance is compounded by its ability to form biofilms, dense bacterial communities that are challenging to eliminate via standard antibiotic therapies. As such, targeting biofilm formation is considered a viable strategy for addressing these infections. This study assessed the effectiveness of surfactin, a cyclic lipopeptide biosurfactant synthesized by Bacillus subtilis natto NTU-18, in preventing biofilm formation by E. faecalis. Analytical characterization of surfactin was performed via liquid chromatography‒mass spectrometry (LC‒MS). Additionally, transcriptomic sequencing and quantitative PCR (qPCR) were used to investigate alterations in E. faecalis gene expression following treatment with surfactin. The data revealed notable suppression of crucial virulence-related genes responsible for pilus construction and exopolysaccharide synthesis, both of which are vital for E. faecalis adhesion and biofilm structure. Functional tests confirmed that surfactin treatment substantially reduced E. faecalis attachment to Caco-2 cell monolayers and curtailed exopolysaccharide production. Moreover, confocal laser scanning microscopy revealed significant thinning of the biofilms. These observations support the potential utility of surfactin as a therapeutic agent to manage biofilm-associated infections caused by E. faecalis.</p>","PeriodicalId":9233,"journal":{"name":"BMC Microbiology","volume":"25 1","pages":"85"},"PeriodicalIF":4.0000,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11852883/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"BMC Microbiology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s12866-025-03786-y","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Enterococcus faecalis is a significant pathogen in healthcare settings and is frequently resistant to multiple antibiotics. This resistance is compounded by its ability to form biofilms, dense bacterial communities that are challenging to eliminate via standard antibiotic therapies. As such, targeting biofilm formation is considered a viable strategy for addressing these infections. This study assessed the effectiveness of surfactin, a cyclic lipopeptide biosurfactant synthesized by Bacillus subtilis natto NTU-18, in preventing biofilm formation by E. faecalis. Analytical characterization of surfactin was performed via liquid chromatography‒mass spectrometry (LC‒MS). Additionally, transcriptomic sequencing and quantitative PCR (qPCR) were used to investigate alterations in E. faecalis gene expression following treatment with surfactin. The data revealed notable suppression of crucial virulence-related genes responsible for pilus construction and exopolysaccharide synthesis, both of which are vital for E. faecalis adhesion and biofilm structure. Functional tests confirmed that surfactin treatment substantially reduced E. faecalis attachment to Caco-2 cell monolayers and curtailed exopolysaccharide production. Moreover, confocal laser scanning microscopy revealed significant thinning of the biofilms. These observations support the potential utility of surfactin as a therapeutic agent to manage biofilm-associated infections caused by E. faecalis.
期刊介绍:
BMC Microbiology is an open access, peer-reviewed journal that considers articles on analytical and functional studies of prokaryotic and eukaryotic microorganisms, viruses and small parasites, as well as host and therapeutic responses to them and their interaction with the environment.