Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis - GC-MS Dataset

Raw GC-MS Data associated with the manuscript 'Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis' by Antypas et al. Infective endocarditis (IE) is a life-threatening biofilm-associated infection, yet the factors driving biofilm formation in this setting remain poorly understood. Here, we identified the Fsr quorum sensing (QS) system of Enterococcus faecalis as a potent negative regulator of IE pathogenesis. Using microfluidic and in vivo models, we show that Fsr is induced in late IE when bacteria become shielded from blood flow. Deleting Fsr promoted robust biofilm growth, partly through downregulation of gelE and sprE, reprogrammed metabolism by upregulating lrgAB to enhance pyruvate utilization, and increased gentamicin tolerance in vivo. Furthermore, the Fsr-regulated protease GelE cleaved human pro-IL-1β into a bioactive fragment, suggesting a potential species-specific mechanism for inflammation modulation by QS. Consistent with our pre-clinical findings, analysis of two IE patient cohorts linked naturally occurring Fsr-deficient E. faecalis to prolonged bacteremia and a higher disease severity score. Overall, our findings provide insights into the role of QS in biofilm growth and persistence in IE. This dataset contains the raw data of the gas chromatography-mass spectrometry (GC-MS) analysis, quantifying lactic acid, pyruvic acid and L-alanine in cell pellets (CL) and supernatant (SN) of OG1RF WT, Δfsr, lrgA::Tn, and lrgB::Tn cultured under aerobic (AER) and anaerobic (ANA) conditions. Details of the analyses including sample harvest, metabolite extraction, derivatization, GC-MS settings and metabolite quantification are described in the Material and Methods section of the manuscript. The data was acquired with a 8890 GC System (Agilent Technologies) equipped with a DB5 capillary column (J&W Scientific, 30 m, 250 μm inner diameter, 0.25-μm film thickness, 10-m inert duraguard) connected to a 5977B GC/MSD in electron impact (EI) mode linked to a 7693A autosampler (Agilent Technologies). The files are .D format.

Organizational unit: DSF Lab

Type: Dataset

DOI: 10.26037/yareta:gsciqvezcffqpoxxie5qfy7nyy

License: Creative Commons Public Domain Dedication

Keywords: Enterococcus faecalis, quorum sensing, Metabolism, Pyruvic acid, Gas Chromatography-Mass Spectrometry, Infective endocarditis, Biofilm

Publication date

11/12/2025

Retention date09/12/2035

Access levelPublic

SensitivityBlue

Contract on the use of data

License

Contributors

Kloehn, Joachim

Antypas, Haris

Winter, Cristina Colomer

Kline, Kimberly A.

Files

2 Files (1.3 GB)

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17

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        <datacite:description descriptionType="Abstract" xml:lang="en">Raw GC-MS Data associated with the manuscript 'Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis' by Antypas et al.

Infective endocarditis (IE) is a life-threatening biofilm-associated infection, yet the factors driving biofilm formation in this setting remain poorly understood. Here, we identified the Fsr quorum sensing (QS) system of Enterococcus faecalis as a potent negative regulator of IE pathogenesis. Using microfluidic and in vivo models, we show that Fsr is induced in late IE when bacteria become shielded from blood flow. Deleting Fsr promoted robust biofilm growth, partly through downregulation of gelE and sprE, reprogrammed metabolism by upregulating lrgAB to enhance pyruvate utilization, and increased gentamicin tolerance in vivo. Furthermore, the Fsr-regulated protease GelE cleaved human pro-IL-1β into a bioactive fragment, suggesting a potential species-specific mechanism for inflammation modulation by QS. Consistent with our pre-clinical findings, analysis of two IE patient cohorts linked naturally occurring Fsr-deficient E. faecalis to prolonged bacteremia and a higher disease severity score.  Overall, our findings provide insights into the role of QS in biofilm growth and persistence in IE.

This dataset contains the raw data of the gas chromatography-mass spectrometry (GC-MS) analysis, quantifying lactic acid, pyruvic acid and L-alanine in cell pellets (CL) and supernatant (SN) of OG1RF WT, Δfsr, lrgA::Tn, and lrgB::Tn cultured under aerobic (AER) and anaerobic (ANA) conditions.
Details of the analyses including sample harvest, metabolite extraction, derivatization, GC-MS settings and metabolite quantification are described in the Material and Methods section of the manuscript.
The data was acquired with a 8890 GC System (Agilent Technologies) equipped with a DB5 capillary column (J&amp;W Scientific, 30 m, 250 μm inner diameter, 0.25-μm film thickness, 10-m inert duraguard) connected to a 5977B GC/MSD in electron impact (EI) mode linked to a 7693A autosampler (Agilent Technologies). The files are .D format.


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Metadata version: 5.0

Disposal approval: Yes

Retention expiration: 09/12/2035 00:00:00

Created: 11/12/2025 18:52:13

Deposit: Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis - GC-MS Dataset

Deposit creation

Deposit approval: 11/12/2025 18:52:12

SIP: Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis - GC-MS Dataset

AIP: Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis - GC-MS Dataset

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Agent 5: ClamAV | Software | 1.4.2

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