{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Antypas H"],"funding":["Swiss National Science Foundation","NIAID NIH HHS"],"pubmed_abstract":["Infective endocarditis (IE) is a life-threatening biofilm-associated infection, yet the factors driving biofilm formation remain poorly understood. Here, we identified the Fsr quorum sensing (QS) system of <i>Enterococcus faecalis</i> as a potent negative regulator of IE pathogenesis. Using microfluidic and <i>in vivo</i> models, we show that Fsr is induced in late IE when bacteria become shielded from blood flow. Deleting Fsr altered biofilm metabolism and promoted robust biofilm growth and gentamicin tolerance <i>in vivo</i>. Furthermore, Fsr inactivation attenuated inflammation by disrupting IL-1β cleavage and activation via the Fsr-regulated gelatinase (<i>gelE</i>), allowing biofilm to grow unchecked by the immune system. Consistent with our pre-clinical findings, analysis of two IE p"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2025.02.07.636843"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11839028"],"repository":["biostudies-literature"],"pubmed_title":["Fsr quorum sensing system restricts biofilm growth and activates inflammation in enterococcal infective endocarditis."],"pmcid":["PMC11839028"],"funding_grant_id":["204343","211422","310030","R21 AI164018"],"pubmed_authors":["Neo CJY","Brugger SD","Schmidtchen V","Zinkernagel AS","DA Silva RAG","Ng KKF","Wong JJ","Manzano C","Wong SL","Tan RJW","Tanoto FR","Li Y","Kline KA","Pethe K","Winter CC","Radhesh SM","Antypas H","Staiger WI","Hasse B","VAN Tyne D"],"additional_accession":[]},"is_claimable":false,"name":"Fsr quorum sensing system restricts biofilm growth and activates inflammation in enterococcal infective endocarditis.","description":"Infective endocarditis (IE) is a life-threatening biofilm-associated infection, yet the factors driving biofilm formation remain poorly understood. Here, we identified the Fsr quorum sensing (QS) system of <i>Enterococcus faecalis</i> as a potent negative regulator of IE pathogenesis. Using microfluidic and <i>in vivo</i> models, we show that Fsr is induced in late IE when bacteria become shielded from blood flow. Deleting Fsr altered biofilm metabolism and promoted robust biofilm growth and gentamicin tolerance <i>in vivo</i>. Furthermore, Fsr inactivation attenuated inflammation by disrupting IL-1β cleavage and activation via the Fsr-regulated gelatinase (<i>gelE</i>), allowing biofilm to grow unchecked by the immune system. Consistent with our pre-clinical findings, analysis of two IE p","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Feb","modification":"2026-04-08T19:22:06.862Z","creation":"2025-04-06T23:41:12.917Z"},"accession":"S-EPMC11839028","cross_references":{"pubmed":["39974957"],"doi":["10.1101/2025.02.07.636843"]}}