Relative Contributions of Ebp Pili and the Collagen Adhesin Ace to Host Extracellular Matrix Protein Adherence and Experimental Urinary Tract Infection by Enterococcus faecalis OG1RF Original paper
Researched by:
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Divine Aleru
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Divine Aleru
Read MoreI am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.
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Microbes
Microbes
Microbes are microscopic organisms living in and on the human body, shaping health through digestion, vitamin production, and immune protection. When microbial balance is disrupted, disease can occur. This guide explains key microbe types—bacteria, viruses, fungi, protozoa, and archaea—plus major pathogenic and beneficial examples.
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Divine Aleru
Read More
Researched by:
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Divine Aleru
ID
Divine Aleru
Read More
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Divine Aleru
What was studied?
This study investigated how Ebp pili and the Ace collagen adhesin contribute to Enterococcus faecalis adherence, microbiome colonization, and urinary tract infection. Researchers created gene deletion mutants lacking ebpABC pili genes, ace adhesin, or both, and tested adherence to extracellular matrix proteins and infection severity. They examined collagen, fibrinogen, and host cell adherence, biofilm formation, and infection outcomes in a mouse urinary tract infection model to determine how these virulence factors enable microbiome persistence and pathogenic transition.
Who was studied?
The study examined microbiome-derived and laboratory strains of Enterococcus faecalis, including wild-type OG1RF and mutants lacking pili or adhesin genes. Researchers tested bacterial adherence to host extracellular matrix proteins and host cells, and evaluated infection severity in mice using experimental urinary tract infection models. These models represented gut microbiome colonization, host tissue adherence, and systemic infection conditions relevant to human disease.
What were the most important findings?
Ebp pili and Ace adhesin strongly promoted Enterococcus faecalis adherence, microbiome persistence, and infection severity. Major microbial associations included increased adherence to collagen and fibrinogen, which are key host structural proteins exposed during tissue damage. Deletion of ebpABC reduced fibrinogen adherence by approximately 75% and reduced collagen adherence by up to 79%, confirming pili as major adherence factors. Ace adhesin also strongly promoted collagen binding, and combined deletion caused further adherence loss. Pili deletion reduced biofilm formation by 62%, demonstrating impaired microbiome persistence. In mouse urinary tract infection models, ace and ace-ebpABC mutants showed significantly reduced kidney infection, with bacterial loads reduced by up to 1.9 log compared to wild-type strains. These findings show that pili and adhesins enable Enterococcus to bind host tissues, persist in disrupted microbiomes, and transition into invasive infection.
What are the greatest implications of this study?
This study shows that Enterococcus pili and adhesins function as key microbiome virulence factors that enable tissue adherence, microbiome dominance, and infection development. Increased Enterococcus abundance, collagen adherence, fibrinogen binding, and biofilm formation represent important microbiome signatures associated with infection risk. These mechanisms explain how microbiome disruption allows Enterococcus expansion and systemic infection.
Enterococcus faecalis
Enterococcus faecalis is a gut‑adapted, Gram‑positive, non‑spore‑forming facultative anaerobe that becomes an important opportunistic pathogen in healthcare when host barriers are breached or antibiotics select for enterococcal overgrowth. Its clinical impact is driven more by persistence, adhesion, and biofilm biology, quorum‑regulated secreted effectors (fsr‑controlled gelatinase GelE), and high genome plasticity than by a broad repertoire of classical tissue‑destroying toxins. Antimicrobial decision‑making must account for the intrinsic poor activity of cephalosporins, the potential for transferable glycopeptide resistance mediated by van gene clusters, and the need for regimen selection in endocarditis that respects synergy/tolerance and local high‑level aminoglycoside resistance patterns.