Divine Aleru, Microbiome Signatures Research Coordinator

This study shows that disulfiram, in combination with copper ions, significantly enhances the bactericidal effects against M. tuberculosis, especially against drug-resistant strains. The copper-dependent activity of disulfiram offers a potential new therapeutic approach for tuberculosis.

The promise of copper ionophores as antimicrobials rests on raising intracellular copper to disable core enzymes, restore antibiotic activity, and boost host killing, with clear microbial markers to track response.

This review links the molecular mechanisms of zinc as a pro-antioxidant mediator to lower oxidative stress, restrained inflammation, and clinical signals in elders and chronic disease, with clear mechanistic paths that can inform microbiome interpretation.

This review maps zinc in human health and infectious diseases, linking host zinc control to pathogen survival, clinical trial signals, and simple gene and protein markers that explain microbiome shifts under zinc pressure.

Current biomedical use of copper chelation therapy spans Wilson’s disease, cancer, lung fibrosis, diabetes, and neurodegeneration, with strongest support in Wilson’s disease and emerging roles in oncology and fibrosis, while neuro data remain limited.

Restricting iron import makes bacteria far more sensitive to copper, enabling strong antimicrobial effects at lower doses and revealing gene and enzyme signatures that inform microbiome-aware control strategies.

Wound dressings impregnated with cuprous oxide cut bioburden fast, block bacterial passage, and act against common wound microbes with durable activity, offering a practical tool to reshape the wound microbiome in support of healing.

This case study highlights the difficulty of diagnosing Wilson’s disease in a patient with psychiatric and gastrointestinal symptoms. It underscores the importance of considering Wilson’s disease when unexplained liver dysfunction and neurological symptoms are present, advocating for comprehensive diagnostic approaches.

This study explores the effects of copper exposure on copper and antibiotic resistance genes during swine manure composting, revealing changes in microbial community composition and gene persistence, particularly at higher copper concentrations, with implications for environmental management and resistance gene spread.

This study investigates how copper supplementation affects gut microbiota and E. coli resistance in weaned piglets. It reveals that copper alters microbial composition and promotes antibiotic resistance, with potential implications for public health and animal agriculture.

The study highlights the crucial role of the copA copper efflux system in the virulence of Streptococcus pneumoniae by protecting it from macrophage-mediated copper toxicity, a key immune defense.

This study highlights how bacterial sensors for zinc and cobalt operate under tightly regulated metal conditions. It reveals how improper sensing during metal shock can compromise bacterial function, offering insights into potential therapeutic strategies that exploit bacterial vulnerabilities.

Nickel exposure reduces enterobactin production in Escherichia coli, extends lag phase, triggers iron-starvation signals, and lowers extracellular catechols, defining gene and metal markers to track iron supply in Enterobacterales.

This review shows non-classical siderophore roles in copper and zinc handling, oxidative stress control, and signaling, and maps gene–host markers that predict pathogen fitness across urine, gut, and airway.

Yersiniabactin binds copper in vivo, protects UPEC from copper stress, and blocks catecholate-driven Cu(II)→Cu(I) toxicity, yielding a clear urinary microbiome signature with direct clinical use.

The review links copper’s enzyme roles and tight homeostasis to clinical states that shift metal supply at mucosa, offering host and microbial markers to track copper-shaped microbiome risk.

Mycobacterium tuberculosis and copper shows copper rises at infection sites, while bacterial systems (MctB, CsoR–CtpV, RicR–MymT/MmcO) defend against toxicity; these markers inform clinical risk and target discovery.

This original study tested the Role of calprotectin in withholding zinc and copper from Candida albicans and defined when this host protein blocks metal nutrition to shape fungal survival. The authors asked if calprotectin (the S100A8/S100A9 complex) depletes bioavailable Zn and Cu around the fungus, how C. albicans adapts its metal uptake […]

Copper resistance is essential for virulence of Mycobacterium tuberculosis; MctB prevents copper build-up, and loss of MctB cripples survival in copper-rich granulomas, defining actionable microbial and host signatures.

The cuprous oxidase activity of CueO converts toxic Cu(I) to Cu(II) in E. coli, partners with CopA and CusCFBA, and marks copper-tolerant Enterobacterales that can persist in acidic, inflamed gut niches.

Copper homeostasis in Enterococcus hirae maps a four-gene circuit—CopA, CopB, CopY, CopZ—and a reductase that set copper uptake and export, yielding clear genomic markers to predict copper tolerance and stress in gut and wound niches.

CtpB tailors Mycobacterium tuberculosis growth to copper-limited niches, boosts fitness in adipocytes, and raises copper stress risk during phagosomal surges, yielding a clear gene–niche signature for clinical use.

Host subversion of bacterial metallophore usage shows that zinc starvation makes S. aureus import copper via staphylopine, triggering copper stress and reducing fitness in vivo; these loci and host calprotectin form a practical microbiome signature.

The extracellular metallometabolome links secreted metallophores and ionophores to metal control at mucosa, explaining microbiome shifts, pathogen fitness, and host defense, with clear genomic markers for clinical use.