Manganese acquisition is essential for virulence of Enterococcus faecalis 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:
-
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 examined the role of manganese (Mn) acquisition in the virulence of Enterococcus faecalis. Researchers identified and characterized the key manganese transport systems in E. faecalis, focusing on the ABC-type transporter EfaCBA and two Nramp-type transporters, MntH1 and MntH2. They tested how these transport systems contribute to bacterial growth in manganese-limited environments and the impact of their inactivation on virulence in several infection models.
Who was studied?
The study analyzed Enterococcus faecalis strain OG1RF and its mutants, which lacked one or more of the manganese transporters (EfaCBA, MntH1, and MntH2). These mutants were tested for growth under manganese-restricted conditions, as well as in infection models involving Galleria mellonella larvae, rabbit endocarditis, and murine catheter-associated urinary tract infection (CAUTI).
What were the most important findings?
The study demonstrated that manganese acquisition is critical for Enterococcus faecalis virulence. The triple mutant strain lacking EfaCBA, MntH1, and MntH2 showed a >95% reduction in cellular manganese content and exhibited severe growth defects in manganese-limited environments. The triple mutant was virtually avirulent in multiple animal models, including Galleria mellonella and rabbit endocarditis. In contrast, strains with single or double deletions of these transporters exhibited reduced but not complete loss of virulence. Furthermore, inactivation of MntH2, in particular, resulted in increased sensitivity to the host protein calprotectin, a manganese-sequestering antimicrobial factor. This study underscores the essential role of manganese in E. faecalis pathogenesis and its potential as a therapeutic target.
What are the greatest implications of this study?
This study highlights that manganese acquisition is vital for Enterococcus faecalis to thrive in the host environment and cause infection. The findings suggest that targeting manganese transport systems could be an effective strategy for developing new antimicrobial treatments to combat E. faecalis infections, particularly in cases where the pathogen exhibits resistance to conventional antibiotics.
Manganese (Mn)
Manganese plays a pivotal role in microbial pathogenesis. As a vital cofactor for enzymes involved in antioxidant defense and metabolism, manganese is essential for pathogens, enabling them to survive within the host. However, when not properly managed, manganese can become toxic to both the host and the pathogen. The host’s immune system, through mechanisms like the secretion of calprotectin, tries to limit microbial access to manganese, creating an ongoing battle between host defenses and microbial survival .
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.