Divine Aleru, Microbiome Medicine Research Coordinator

Among 52 women, those with polycystic ovary syndrome plus dyslipidemia showed more Bacteroidota and Clostridium_sensu_stricto_1 and less Faecalibacterium and Holdemanella, and these butyrate-linked genera correlated inversely with triglyceride and cholesterol levels.

Combined gut bacteriome, mycobiome, and serum metabolome profiling distinguished PCOS patients from healthy individuals across BMI categories, with a metabolite-based classifier achieving perfect discriminatory accuracy.

Japanese women with premenstrual syndrome had a distinct gut microbiota, and the genus Collinsella was about 4.5 times more abundant than in controls (3.96% versus 0.88%), suggesting diet-based interventions targeting it may help.

Women with polycystic ovary syndrome had significantly lower gut fungal diversity than healthy controls, with a distinct mycobiota community structure and shifts in fungal composition at the phylum, family and genus levels.

In a rat model of primary dysmenorrhea, a graphene-based warm-uterus acupoint paste reduced writhing and uterine inflammation while raising gut Lactobacillus and lowering Romboutsia, alongside shifts in 32 fecal metabolites.

Women with menopausal syndrome showed gut microbiota dysbiosis, with 14 species differing from healthy menopausal women. Aggregatibacter segnis, Bifidobacterium animalis, and Acinetobacter guillouiae were depleted and tracked positively with estradiol and negatively with FSH and LH.

In 22 women with primary ovarian failure versus 29 controls, the vaginal microbiota was more diverse with reduced Lactobacillus, and a 34-genus signature predicted the condition with an AUC of 0.841, while two Lactobacillus species showed opposite associations with reproductive hormones.

PCOS disrupted the normal 24-hour diurnal rhythm of salivary microbiota abundance seen in healthy women.

Endometriosis involves ectopic endometrial tissue causing pain and infertility. Validated and Promising Interventions include Hyperbaric Oxygen Therapy (HBOT), Low Nickel Diet, and Metronidazole therapy.

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.

Enterococcus faecium (VREfm) has become a major healthcare threat due to its ability to acquire resistance and adapt to both clinical and environmental conditions. This review calls for new strategies to combat VREfm, emphasizing its transmission through multiple routes and the need for better diagnostic and treatment approaches.

Enterococcus faecalis utilizes five distinct iron uptake systems, including novel transporters, to maintain iron homeostasis and support virulence. Heme acquisition also plays a critical role in its pathogenesis. Targeting these transporters offers a promising approach for treating E. faecalis infections.

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 […]

This study examined the Fsr quorum-sensing system in Enterococcus faecalis and its role in regulating the surface display of the collagen-binding protein Ace, a key virulence factor. Researchers investigated how disruption of the Fsr system, as well as GelE protease activity, influenced the expression of Ace on the cell surface, its ability […]

Enterococcus faecium adapts through gene transfer and resistance mechanisms, making it a major cause of hospital infections. The study emphasizes the importance of genomic surveillance and the development of novel therapeutics like phage therapy and microbiota-based treatments to control the spread of VREfm infections.

VanB Enterococcus strains show inducible vancomycin resistance, enabling microbiome persistence and infection risk. Diagnostic methods reliably detect resistant strains, but low-level resistance may be missed. Enterococcus resistance expansion represents a key microbiome signature associated with hospital infection and treatment failure.

This review examined how Enterococcus faecalis and Enterococcus faecium regulate VanA- and VanB-type glycopeptide resistance, which enables survival during vancomycin and related antibiotic exposure. The authors reviewed molecular, genetic, and microbiological evidence explaining how resistance genes alter peptidoglycan synthesis and how regulatory systems activate resistance in response to antibiotic exposure. The review […]

This review examined how Enterococcus faecalis and Enterococcus faecium adapt to the gut microbiome, hospital environments, and host tissues through genetic plasticity, antimicrobial resistance, and virulence factor acquisition. The authors reviewed microbiological, genomic, and clinical evidence explaining how Enterococcus survives environmental stress, acquires resistance genes, and transitions from a gut microbiome commensal […]

Enterococcus develops antibiotic resistance through genetic adaptation, enabling microbiome dominance and infection persistence. Resistance mechanisms allow Enterococcus to survive antibiotic exposure, expand in the gut microbiome, and spread resistance genes, making Enterococcus expansion a key microbiome signature linked to infection risk and antimicrobial resistance.

Enterococcus faecalis uses pheromone signaling to detect microbiome conditions, transfer antibiotic resistance genes, and activate virulence. This system promotes microbiome persistence, bacterial aggregation, and infection risk, making pheromone signaling an important microbiome signature of Enterococcus pathogenicity.

Enterococcus faecalis pili and adhesins enable microbiome persistence, collagen adherence, biofilm formation, and urinary tract infection. Loss of these factors reduces microbiome colonization and infection severity, identifying pili and adhesins as key microbiome virulence signatures linked to infection risk.

This review shows that Enterococcus expands during microbiome disruption, forms polymicrobial biofilms, and activates virulence factors that promote colonization, immune evasion, and systemic infection, identifying Enterococcus as a microbiome-driven pathobiont linked to increased infection risk and poor clinical outcomes.

Cytolysin allows Enterococcus faecalis to disrupt the microbiome, kill competitors, evade immune defenses, and increase infection severity. This toxin promotes microbial imbalance, pathogen expansion, and systemic infection, making cytolysin a key microbiome virulence factor and clinical biomarker.

Enterococcus faecalis regulates immune tolerance and microbiome stability but becomes pathogenic during dysbiosis. It increases IgA production, modulates inflammatory signaling, and strengthens gut barrier function in eubiosis. In dysbiosis, it expands, evades immune clearance, promotes inflammation, and contributes to systemic infections, making it a key microbiome biomarker of immune and microbial imbalance.