Divine Aleru, Microbiome Medicine Research Coordinator

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.

This review explores copper’s essential roles in human health and its involvement in diseases like Wilson’s disease, Alzheimer’s, and cancer. It highlights copper’s dual role in disease progression and therapeutic strategies for copper imbalances.

This review highlights the complex relationship between copper metabolism and microbial infections. It focuses on the role of copper transporters ATP7A/B in regulating copper homeostasis and how microbes manipulate these mechanisms to survive in the host.

The study explores how gastrointestinal pH affects copper solubility and speciation during digestion. It reveals the role of food components in modulating copper bioavailability and highlights the impact of pH on copper toxicity and absorption.

This study highlights how Cu imbalance leads to oxidative stress and cellular toxicity, contributing to liver and neurological diseases. It emphasizes the need for tight Cu regulation and offers insights into potential biomarkers and therapeutic strategies for Cu-related disorders.

This study examines the copper-binding properties of Hist-5, a salivary peptide, and its role in combating Candida albicans infections. The findings highlight the critical role of copper ions in enhancing the peptide’s antimicrobial activity through specific metal-binding motifs.

Copper-dependent activity against Candida albicans rises when histatin peptides bind copper via a proximal bis-His site, lowering EC50 and improving killing in vitro; copper chelation reverses this effect.

Dietary copper-fructose interactions in rats depleted Akkermansia, shifted Firmicutes families, weakened tight junctions and goblet cells, and raised liver injury signals, defining a dysbiosis–barrier–liver axis.

Dietary copper effect on intestinal microbiota in weaned piglets increased E. coli abundance and raised ciprofloxacin and chloramphenicol resistance, while shifting key metabolic pathways without growth benefit.

Copper and zinc toxicity in innate immunity drives early control of bacterial pathogens and shapes mucosal niches. The review links host metal routing and microbial export genes to killing, virulence, and microbiome shifts.

Copper treatment of sepsis links host copper delivery, microbial copper genes, and cell death pathways. The review highlights biomarker value and careful therapeutic targeting to aid control of infection while limiting tissue injury.

This review explores the critical role of copper in microbial pathogenesis, focusing on how the host uses it as an antimicrobial weapon and how pathogens resist Cu toxicity. It suggests potential therapeutic avenues targeting Cu resistance mechanisms.

This review explores copper’s role in microbial pathogenesis, highlighting its use by hosts as an antimicrobial weapon and the resistance mechanisms developed by pathogens. It discusses copper’s involvement in immune defense and fungal virulence, offering insights into potential therapeutic strategies.

This review discusses advancements in chelation therapy for treating metal toxicity, focusing on chelating agents, combination therapies, and antioxidants. Key findings highlight the effectiveness of MiADMSA and the potential for improved treatments.

This review discusses the detrimental effects of lead (Pb) exposure on gut microbiota, metabolism, and homeostasis, highlighting its role in metabolic and systemic disorders. It suggests interventions such as probiotics and dietary supplementation for mitigating Pb toxicity.

This study explores how lead exposure disrupts gut microbiota, leading to compromised gut health and systemic issues. It highlights the potential of probiotics and other interventions to restore balance and mitigate Pb toxicity.

The study investigates the effects of DNase I and proteinase K on the structure and composition of multispecies oral biofilms, finding that these enzymes disrupt biofilm integrity and shift microbial composition, potentially enhancing the effectiveness of antimicrobial treatments.