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Updated: Jan 25, 2026
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Opsonophagocytic Killing Assay to Assess Immunological Responses Against Bacterial Pathogens
Published on: April 5, 2019
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Enterococcus faecalis Gluconate Phosphotransferase System Accelerates Experimental Colitis and Bacterial Killing by
Ting-Jia Fan1,2, Laura Goeser1, Arash Naziripour1
1Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Infection and Immunity
|May 1, 2019
Summary
Enterococcus faecalis uses a specific phosphotransferase system (PTS) to grow on gluconate. This system does not aid intestinal colonization but exacerbates colitis and inflammation by enhancing bacterial survival and cytokine release.
Area of Science:
- Microbiology
- Gastroenterology
- Immunology
Background:
- Enterococcus faecalis is an intestinal bacterium linked to infections, inflammatory bowel diseases, and colon cancer.
- The factors influencing E. faecalis intestinal colonization are not fully understood.
- A specific phosphotransferase system (PTS) in E. faecalis OG1RF, involving genes OG1RF_12399-12402, is implicated in gluconate metabolism.
Purpose of the Study:
- To investigate the role of the E. faecalis PTS gluconate pathway in bacterial growth, intestinal colonization, and colitis.
- To determine if this PTS facilitates E. faecalis intestinal colonization and exacerbates colitis.
- To elucidate the impact of the PTS on bacterial survival within host cells and inflammatory responses.
Main Methods:
- Generated E. faecalis strains with mutations in the PTS genes (OG1RF_12399-12402).
- Assessed bacterial growth in minimal media with varying carbohydrates.
- Measured PTS gene expression in response to gluconate.
- Colonized germfree mice (wild-type and IL-10 deficient) with E. faecalis consortia.
- Infected cell lines (macrophages, intestinal epithelial cells) with E. faecalis.
- Quantified bacterial abundance, inflammation, cytokine secretion, and intracellular survival.
Main Results:
- E. faecalis upregulates OG1RF_12399 transcription in the presence of gluconate.
- Mutant E. faecalis strains lacking functional PTS genes cannot grow in gluconate-containing media.
- The PTS is not essential for E. faecalis intestinal colonization in mice.
- The PTS is associated with accelerated colitis onset in IL-10 deficient mice.
- The PTS enhances E. faecalis survival within macrophages and increases pro-inflammatory cytokine secretion.
Conclusions:
- The E. faecalis PTS gluconate system is crucial for growth on gluconate but not for intestinal colonization.
- This PTS contributes to colitis pathogenesis by promoting bacterial survival and host inflammatory responses.
- Targeting bacterial carbohydrate metabolism, specifically the E. faecalis PTS-gluconate pathway, may offer new therapeutic strategies for inflammatory diseases.
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