Divine Aleru, Microbiome Signatures Research Coordinator

The study investigates how soft metals like silver, mercury, cadmium, and zinc damage bacterial dehydratases by targeting their [4Fe-4S] clusters, revealing insights into the molecular mechanisms of metal toxicity in E. coli. The findings highlight the potential for oxidative stress and inform strategies for antimicrobial resistance.

This study examines the effects of cadmium exposure on the microbiome, showing how it alters gut and blood microbiota, impacts metabolites, and links to inflammatory responses. The research reveals significant microbial shifts and potential biomarkers for Cd-induced toxicity.

Microbial metallophores are vital in sustainable agriculture, enhancing nutrient availability, promoting plant growth, and mitigating heavy metal toxicity. The study highlights their potential in bioremediation and as biocontrol agents.

The study explores the multifaceted role of bacterial siderophores in microbial community dynamics and host interactions. It highlights their impact on bacterial competition, survival, and virulence, offering insights into potential therapeutic strategies for managing infections and manipulating microbial communities.

This study shows that cadmium acts as a zinc mimetic by binding to and activating the HIZR-1 nuclear receptor, leading to the activation of high zinc homeostasis genes in C. elegans. The research highlights the overlap between cadmium and zinc responses, shedding light on cadmium’s transcriptional control mechanisms.

This study explored the role of metallothionein in cadmium toxicity, focusing on its protective and transport roles, particularly in the kidneys. It emphasizes the potential of MT-related biomarkers for assessing cadmium exposure risks in humans.

This study explored how the CzcRS3 two-component system regulates cadmium resistance in P. putida by controlling efflux pump gene expression. The findings emphasize the role of CadR in regulating this system and offer insights into potential bioremediation strategies.

This study investigates the role of ZntA in zinc and cadmium homeostasis, oxidative stress resistance, and virulence in Vibrio parahaemolyticus. ZntA protects against metal toxicity and promotes bacterial survival under stressful conditions, highlighting its importance in bacterial pathogenesis.

This study identifies CadC as a key transcriptional regulator of the cadmium resistance operon in S. aureus plasmid pI258, revealing its role in controlling cadA expression in response to metal ions like cadmium, bismuth, and lead.

The study identifies and characterizes the cadmium resistance operon in S. aureus ATCC12600. It reveals that the cadC gene is crucial for cadmium efflux and resistance but does not function as a repressor, offering new insights into cadmium resistance mechanisms.

This study explores how cadmium binds to human serum transferrin, albumin, and citrate, revealing key insights into cadmium transport and bioavailability in the bloodstream. It also highlights the potential clinical implications for understanding cadmium toxicity and therapeutic interventions.

This study investigates how albumin influences cadmium uptake in primary rat hepatocytes, revealing its protective role in reducing toxicity. The findings suggest albumin’s involvement in cadmium bioavailability and provide insights for developing therapeutic strategies to mitigate cadmium-related health risks.

The review examines the complex role of hydrogen sulfide in modulating the gut microbiome, highlighting its potential as a therapeutic agent to stabilize microbiota biofilms and reduce inflammation in diseases like IBD.

The study explored how gut microbes and chelating agents influence the bioavailability of arsenic, cadmium, lead, and mercury by assessing their intestinal permeability using a Caco-2 cell model. It found that both microbes and chelating agents reduce the permeability of these metals, mitigating their toxicity.

This study explores how altering gastric pH with omeprazole and cimetidine affects cadmium absorption from the diet and its accumulation in murine tissues, showing limited impact on tissue cadmium levels despite changes in gastric pH.

This review explores the toxic effects of cadmium exposure on multiple organ systems and its link to various diseases, including cancer and kidney dysfunction. It also discusses treatment options, including chelation therapy and nanoparticle-based interventions.

This study explores how cadmium disrupts the immune function of macrophages by inhibiting the NF-κB signaling pathway, impairing the response to LPS, and potentially contributing to immune dysfunction in diseases like COPD.

Cadmium exposure inhibits macrophage immune function through suppression of the NF-κB pathway, impairing the response to LPS. This may contribute to immune dysfunction and increased susceptibility to infections, especially in COPD patients.

The study demonstrates how cadmium exposure enhances antibiotic resistance in Salmonella enterica serovar Typhi by altering bacterial growth, biofilm formation, and antibiotic susceptibility. The findings highlight the environmental impact of cadmium in promoting resistance.

This review highlights how heavy metals alter the gut microbiota and discusses the potential of probiotics to mitigate these effects. It also emphasizes the role of advanced biosensors in detecting heavy metals in urine, supporting real-time monitoring of detoxification processes.

The study investigates how cadmium exposure alters gut and blood microbiomes in rats, linking these changes to metabolic disruptions and systemic inflammation.

This study reveals how cadmium and arsenic exposure via the food chain disrupts oxidative enzyme activity in rats, leading to significant health risks, particularly in the liver and kidneys.

The study uncovers how cadmium disrupts transition metal homeostasis in Streptococcus pneumoniae, affecting manganese and zinc uptake and contributing to oxidative stress.

Cadmium (Cd) is a highly toxic heavy metal commonly found in industrial, agricultural, and environmental settings. Exposure to cadmium can occur through contaminated water, food, soil, and air, and it has been linked to a variety of health issues, including kidney damage, osteoporosis, and cancer. In agriculture, cadmium is often present in phosphate fertilizers and can accumulate in plants, entering the food chain. Its toxicity to living organisms makes cadmium a subject of regulatory concern worldwide, particularly in industrial waste disposal and environmental monitoring.

Fecal microbiota transplantation (FMT) has demonstrated high success in treating recurrent Clostridium difficile infection, with potential benefits for other gastrointestinal disorders, including IBD, obesity, and metabolic syndrome. FMT restores microbial diversity,

This review explores the role of chelation therapy in treating arsenic and mercury poisoning, focusing on the efficacy of BAL, DMPS, and DMSA in acute cases and the challenges posed by chronic exposure. It discusses therapeutic benefits, limitations, and the need for further research.

This review explores the protective effects of selenium against arsenic and cadmium toxicity, emphasizing its role in reducing oxidative stress, inflammation, and cellular damage. The findings suggest selenium supplementation may help mitigate the harmful effects of these metals on human health.

This study explores the effects of chronic arsenic exposure on the gut microbiota and bile acid metabolism in mice, revealing significant changes in microbial composition and bile acid homeostasis, which may contribute to metabolic dysfunction and related diseases.

The study explored the impact of arsenic exposure on red blood cell parameters in rural Bangladesh, identifying sex-specific effects and changes in MCV and MCH, which may contribute to anemia or macrocytosis.

The study explored the impact of arsenic exposure on the gut microbiome and host metabolism. The results demonstrated significant changes in microbial composition, which were linked to alterations in metabolic pathways, particularly nitrogen metabolism, shedding light on arsenic’s role in disease promotion.

This study explores the sex-specific effects of chronic arsenic exposure on stromal cells and signaling in the small intestine, highlighting how arsenic disrupts trophocytes and telocytes, which regulate stem cell functions.

The study assessed arsenic exposure in Shanyin County residents through saliva and urine samples. It confirmed that saliva is a potential biomarker for total arsenic exposure, although less effective for understanding arsenic metabolism.

What was studied?This study focused on evaluating arsenic exposure through diet by assessing stool samples in populations from West Bengal, India. Given that arsenic exposure via drinking water is well-documented, the researchers aimed to explore whether stool could serve as a reliable biomarker for arsenic exposure through the food chain, particularly in areas where groundwater […]

The study examines biomarkers of inorganic arsenic exposure in humans, focusing on the metabolism and toxicological effects of arsenic. Key findings include the importance of urinary arsenic measurements and the impact of genetic differences in arsenic metabolism.

The study demonstrates how IL-10 gene knockout mice show significant changes in their gut microbiome and arsenic metabolism. These alterations contribute to higher levels of toxic arsenic metabolites, highlighting the role of host genetics in shaping exposure outcomes.

Arsenic exposure perturbs the gut microbiome in mice and rewires fecal, urinary, and plasma metabolites, including sharp shifts in indole and bile acid pathways, alongside loss of several Firmicutes families and a rise in a Clostridiales group, before any histologic injury appears.

At 100 ppb, arsenic reshaped mouse gut communities, lowered SCFA gene capacity, increased LPS and stress pathways, and enriched multidrug and conjugation genes while shifting taxa toward Akkermansia and Bifidobacterium and away from SCFA-producing Firmicutes.

In rural China, drinking water often exceeded standards, and hair arsenic was higher in exposed residents. Age, male sex, and wheat-based diet increased levels, making hair arsenic a useful long-term marker for clinical screening and for stratifying microbiome studies.

This study highlights the health effects of chronic arsenic exposure through drinking water, linking it to cancers, cardiovascular diseases, and diabetes. It emphasizes the need for monitoring arsenic levels and improving public health interventions.

This study assessed acute and chronic arsenic exposure in an Ethiopian population, finding significant health risks associated with contaminated groundwater and cigarette smoking. Biomarkers like urine and nail arsenic levels were key in understanding exposure.

Long-term exposure to low-level arsenic in drinking water in Mt. Amiata, Italy, was linked to increased mortality and hospitalization risks, especially for cardiovascular diseases and cancer. Even low-level exposure below the regulatory limit showed significant health implications.

This study explores the link between long-term low-level arsenic exposure and diabetes incidence in Denmark. The results suggest a modest association, highlighting the potential health risks of low-level arsenic exposure and the need for further research in this area.

This study evaluates the relationship between arsenic exposure and antibiotic-resistant E. coli carriage in rural Bangladesh, revealing significant associations between arsenic contamination and increased resistance to antibiotics, particularly in children.

The study explores the relationship between arsenic exposure and the infant gut microbiome, revealing sex-specific associations and highlighting how formula-fed male infants are particularly affected. The findings emphasize the importance of early-life environmental exposures on microbiome health and immune development.

This review examines the use of probiotics in managing H. pylori infection, emphasizing their role in enhancing eradication rates, reducing side effects, and restoring gastric microbiota balance. The findings highlight the potential of probiotics as adjuncts to conventional antibiotic therapy.

The study examines how intestinal probiotics restore the intestinal barrier by regulating tight junctions, immune responses, and gut microbiota, offering insights into their therapeutic potential for gut-related diseases.

The study examines how arsenic exposure disrupts erythropoiesis by inhibiting GATA-1 function, leading to anemia. It highlights the role of zinc finger motifs in GATA-1 and provides insights into arsenic-induced hematological disorders.

This review explores the potential for arsenate to replace phosphate in biochemical reactions, examining enzyme promiscuity, arsenate esters’ instability, and the implications for arsenic-based life forms. It also highlights the potential applications in bioremediation and astrobiology.

This review examines arsenic toxicity, its pathways of exposure, and its harmful effects on human health, focusing on oxidative stress, genotoxicity, and epigenetic changes. It highlights the link between arsenic exposure and diseases like cancer, cardiovascular disorders, and neurotoxicity.

This study explores the impact of sulfate-reducing bacteria on arsenic migration and transformation in groundwater. It highlights how sulfate reduction enhances arsenic release and mobilization, providing insights into potential bioremediation strategies for arsenic-contaminated aquifers.

The study reveals that MTF1 mediates the induction of Metallothionein I by arsenic, highlighting the importance of cysteine residues in the activation of MTF1 and its role in arsenic resistance.

This study investigates how arsenic(III) binds to human metallothionein-3, revealing detailed binding kinetics and the role of MT3 in arsenic detoxification. These findings have implications for understanding arsenic poisoning and potential therapeutic strategies.

This review examines how arsenic binds to proteins, disrupting their function and contributing to toxicity and resistance mechanisms. It highlights key proteins like thioredoxin and pyruvate dehydrogenase and discusses implications for arsenic-related diseases and bioremediation strategies.

The study explores how ArsD, a metallochaperone, enhances ArsA’s ability to expel arsenic from cells, improving arsenic detoxification. This interaction increases arsenic resistance in E. coli, with potential applications in bioremediation and combating arsenic poisoning.

This study investigates the structural and biochemical role of ArsD, a metallochaperone in E. coli, in enhancing arsenic detoxification by transferring As(III) to the ArsA ATPase, providing new insights into arsenic resistance mechanisms in bacteria.

This study explored the complex regulatory roles of ArsR proteins in Agrobacterium tumefaciens 5A, showing they influence a broad range of cellular functions, including arsenic resistance, metabolism, and iron homeostasis.

This systematic review links probiotics and heavy metals to clinical outcomes, showing faster diarrhea recovery with zinc, fewer H. pylori therapy side effects, improved iron absorption with prebiotics, and early evidence of lower toxic metal burden in pregnancy.

This review outlines the diversity, evolution, and distribution of arsenic resistance genes in prokaryotes, emphasizing their central role in the environmental microbiome, biogeochemical cycling, and potential clinical implications through gene transfer and resistance in pathogens.

This study demonstrates that both a functional host As3mt enzyme and a stable, diverse gut microbiome—especially the presence of Faecalibacterium prausnitzii—are required for full protection against acute arsenic toxicity in mice, highlighting the microbiome as a target for arsenicosis prevention and treatment.

The human gut microbiome and arsenic toxicity are tightly linked: microbes change arsenic speciation and dose, while arsenic reshapes gut ecology, altering risk. Clinicians should integrate microbiome status, nutrition, antibiotics history, and speciation into assessment and management.

In Nepal, arsenic disturbs the gut microbiome, driving sulfate-reducers and depleting commensals; urine arsenic best explains dysbiosis patterns with clear taxa-level signals useful for exposure-aware clinical care.

Arsenic can disrupt both human health and microbial ecosystems. Its impact on the gut microbiome can lead to dysbiosis, which has been linked to increased disease susceptibility and antimicrobial resistance. Arsenic’s ability to interfere with cellular processes, especially through its interaction with essential metals like phosphate and zinc, exacerbates these effects.

This study shows that probiotics can mitigate the effects of heavy metal toxicity in farmed fish. By binding metals and reducing oxidative stress, probiotics improve fish health and safety for consumption, offering a sustainable solution for the aquaculture industry.

Lactobacillus plantarum CCFM8246 shows protective effects against copper toxicity in mice by promoting copper excretion, alleviating oxidative stress, and improving liver function and cognitive performance. This suggests its potential for use in therapeutic applications for copper toxicity.

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.

What was studied?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 systems, […]

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.