Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence 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 focused on identifying and characterizing the iron uptake mechanisms of Enterococcus faecalis and how these mechanisms contribute to its virulence. Researchers investigated five iron acquisition systems in E. faecalis, including the previously identified transporters (EfaCBA, FeoAB, and FhuDCBG) and two novel ABC-type transporters, FitABCD and EmtABC. The study explored the role of these transporters in maintaining iron homeostasis under iron-depleted conditions and their influence on E. faecalis growth and virulence in various infection models.
Who was studied?
The study examined Enterococcus faecalis strain OG1RF and its mutants, including those lacking individual or combinations of the five iron uptake systems (EfaCBA, FeoAB, FhuDCBG, FitABCD, and EmtABC). These strains were tested in laboratory cultures and infection models, including human serum survival assays, Galleria mellonella larvae, and murine peritonitis and wound infection models. The study also included measurements of intracellular iron content and growth kinetics to assess the contribution of each iron transporter to E. faecalis survival and virulence.
What were the most important findings?
The study found that E. faecalis uses multiple, redundant iron uptake systems to maintain iron homeostasis, with five distinct transporters collectively contributing to virulence. Inactivation of individual transporters had minimal effects on growth under iron-replete conditions, but the absence of multiple systems, particularly in the quintuple mutant (D5Fe), severely impaired growth in iron-depleted environments. Interestingly, E. faecalis also utilized heme as an alternative iron source, which restored growth and virulence in the D5Fe strain under iron-limiting conditions. In vivo models showed that the D5Fe strain was less virulent, especially in systemic infections, indicating that iron acquisition through these systems is critical for E. faecalis pathogenesis. The findings also suggested that the dual role of EfaCBA in both iron and manganese uptake is essential for optimal bacterial function.
What are the greatest implications of this study?
This study underscores the importance of iron acquisition systems in Enterococcus faecalis survival and virulence. The redundancy of these systems highlights the pathogen’s ability to thrive in iron-limited environments within the host. Targeting iron uptake mechanisms, especially heme acquisition, presents a potential therapeutic strategy to combat E. faecalis infections, particularly in patients with compromised immune systems or those affected by hospital-acquired infections.
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.