Divine Aleru, Microbiome Signatures Research Coordinator

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.

Copper serves as both a vital nutrient and a potential toxin, with its regulation having profound effects on microbial pathogenesis and immune responses. In the body, copper interacts with pathogens, either supporting essential enzyme functions or hindering microbial growth through its toxicity. The gastrointestinal tract, immune cells, and bloodstream are key sites where copper plays a crucial role in controlling infection and maintaining microbial balance. Understanding copper’s interactions with the microbiome and host defenses allows for targeted clinical 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.

This study investigates EPS-rich biofilm dynamics, showing how biofilm dispersal via DNase and EPS-glycosidases influences microbial community structure and resilience. It highlights the role of commensal reseeding in restoring microbial balance after dispersal.

This study demonstrates that Vibrio harveyi regulates lead precipitation through quorum-sensing systems, particularly AI1, AI2, and a newly discovered AI3, with implications for environmental bioremediation and microbial interactions in metal-contaminated environments.

This study demonstrates that Cd(II) and Pb(II) induce zntA expression in E. coli through ZntR, highlighting the importance of ZntA in metal resistance and the potential for therapeutic applications targeting metal transporters.

The study of the Ralstonia metallidurans pbr operon reveals mechanisms of lead resistance, highlighting Pb(II) uptake, efflux, and sequestration, and offering potential applications in bioremediation and therapeutic strategies for lead poisoning.

This review defines how lead binding in proteins drives host enzyme inhibition and signaling errors while microbial operons export and precipitate Pb(II), reshaping niche metal availability and competitive fitness.

A comprehensive review of Deferoxamine B metal chelator links siderophore chemistry, microbial uptake, and clinical chelation/imaging, highlighting speciation across metals—including Pb(II)—and implications for microbiome-related metal competition.

An in vivo radiotracer study defines lead absorption and excretion in the rat: duodenal, bile-modulated uptake; competition with Fe/Zn/Ca; iron deficiency–enhanced absorption; erythrocyte transport; early renal–hepatic handling; biliary plus urinary clearance; and bone storage.

A mechanistic review links heavy metals and human health to dysbiosis via protein-binding competition, redox injury, epithelial leak, and LPS-driven inflammation, outlining organ toxicity and clinical chelation strategies.

This review discusses the toxicological impact of heavy metals like arsenic, cadmium, and mercury on human health, particularly their interaction with proteins and enzymes, leading to various disorders and potential carcinogenesis. Detoxification strategies and the importance of environmental cleanup are also highlighted.

The study highlights the cooperation between the PbrA efflux pump and PbrB phosphatase in the detoxification of lead, uncovering a novel mechanism for lead resistance in Cupriavidus metallidurans. This research suggests potential bioremediation applications and deeper insights into microbial heavy metal resistance mechanisms.

This study sheds light on the molecular mechanisms through which Cupriavidus metallidurans CH34 regulates lead resistance, highlighting the role of the PbrR protein and its interaction with the PpbrA promoter in response to Pb(II).

This study demonstrates that lead exposure disrupts the gut microbiome, reducing microbial diversity and impairing key metabolic pathways related to vitamin E, bile acids, nitrogen metabolism, and energy metabolism. These disruptions may contribute to lead toxicity and associated diseases.

This review maps mechanisms and taxa underlying lead bioremediation by bacteria, linking microbial toolkits (EPS, phosphatases, sulfate reducers, PIB-ATPases, metallothioneins) to field performance and clinical microbiome relevance, and guiding signature curation and remediation design.

The review examines the neurotoxic effects of lead exposure, focusing on mechanisms such as ion mimicry, mitochondrial dysfunction, and neuroinflammation. It emphasizes the long-term impact of lead on cognitive function and behavior and discusses biomarkers for assessing lead exposure and its effects on the brain.

This review explores the molecular mechanisms of lead neurotoxicity, focusing on ion mimicry, mitochondrial dysfunction, oxidative stress, and neuroinflammation. The findings emphasize the long-term cognitive and behavioral effects of lead exposure, with implications for clinical intervention and microbiome-related research.

The review highlights the connection between lead exposure and osteoporosis risk in post-menopausal women, showing how lead release during bone turnover contributes to health complications. Strategies to reduce bone resorption during menopause can mitigate lead-related risks and improve health outcomes.

CDC lowered the pediatric BLRV to 3.5 µg/dL, enabling earlier action, clarifying disparities, and setting exposure tiers that should guide microbiome signature curation at contemporary low BLLs.

Meta-analysis shows ALAD polymorphism and lead interactions: ALAD2 raises BLL in workers, lowers chelatable lead, and slightly improves heme indices; bone lead is unchanged.

Clinician summary of prenatal lead exposure and gut microbiome links at age 9–11 in PROGRESS: negative mixture effects, trimester-specific taxa shifts, and a potential second-trimester sensitivity window.

A clinician-focused review updates present-day lead exposure risks and microbiome implications, contrasting older population metrics with SPHERL’s prospective data and outlining how exposure tiers, co-exposures, and confounding shape credible microbiome–lead signatures.

Lead exposure has a profound effect on the microbiome, disrupting microbial diversity, immune responses, and contributing to the development of antimicrobial resistance (AMR). Understanding how Pb interacts with microbial communities and impacts host-pathogen dynamics is essential for clinicians to mitigate long-term health risks and improve treatment strategies.

Ospemifene is an effective and safe treatment for menopausal vaginal dryness and dyspareunia, particularly in women with contraindications for estrogen therapy. It improves vaginal health without significantly affecting systemic hormone levels, providing an alternative treatment for genitourinary syndrome of menopause.

Ospemifene (60 mg/day) significantly reduces dyspareunia and improves vaginal health in postmenopausal women with vulvar and vaginal atrophy. It offers a non-estrogenic treatment option, especially for women who cannot use traditional hormone therapies.

What was studied?This study examined the systemic and local effects of vaginal dehydroepiandrosterone (DHEA) in postmenopausal women, particularly those with a history of breast or gynecologic cancer. It evaluated the impact of vaginal DHEA on hormone concentrations, markers of bone formation, and vaginal cytology, including pH and maturation index. The study aimed to assess the […]

This review underscores the importance of nutrition in managing menopausal symptoms and preventing chronic diseases. It highlights key nutrients such as calcium, vitamin D, and protein and promotes a balanced diet and regular physical activity as integral parts of menopausal health management.

This study reveals that higher levels of physical activity, especially during leisure time, are linked to reduced severity of menopausal symptoms, particularly urogenital and somato-vegetative issues. It suggests incorporating physical activity into the management plan for menopausal women, particularly postmenopausal women.

This review and meta-analysis demonstrate that psychological interventions, such as CBT, MBT, and BT, can significantly reduce hot flash bother and menopausal symptoms. These findings are especially relevant for breast cancer survivors, offering a safe, non-hormonal alternative to HRT.

Veozah (fezolinetant) is an effective non-hormonal treatment for menopause-related vasomotor symptoms. It works by targeting the neurokinin 3 receptor and offers a promising alternative to estrogen therapy with minimal side effects, making it suitable for women with contraindications to hormone treatments.

This study demonstrates that gabapentin 300 mg/day is as effective as estrogen 0.625 mg/day for reducing hot flashes in post-menopausal women. It provides a viable non-hormonal alternative with fewer side effects, making it a good option for women unable or unwilling to take estrogen.

This review confirms that SSRIs and SNRIs, particularly paroxetine and venlafaxine, are effective for managing hot flashes in menopausal women. These therapies provide an alternative to hormone replacement therapy, with minimal side effects and considerations for women with specific health concerns, like hypertension or a history of breast cancer.

This review assesses the safety of vaginal hormones and SERMs in treating genitourinary menopausal symptoms in breast cancer survivors. It finds no significant rise in serum estrogen levels or an increased risk of breast cancer recurrence, but more extensive studies are needed to confirm these findings.

This review highlights the lack of conclusive evidence on the safety of hormone replacement therapy (HRT) in women treated for early-stage endometrial cancer. While a small study found no significant increase in cancer recurrence risk, the low quality of the evidence leaves uncertainty about the benefits and risks of HRT use in these women.

This study shows that menopausal hormone therapy increases the risk of gallstones, especially with topical estrogen and tibolone. However, no increased risk for gallbladder cancer was found. These findings underscore the need for caution in prescribing hormone therapy, particularly for women with higher gallstone risk factors.

Long-term use of estrogen and estrogen-progestin therapies significantly increases the risk of endometrial cancer, particularly for women with lower BMI. The risk is dose-dependent, with continuous-combined therapy having complex effects based on body weight.

This review offers updated guidance on the use of menopausal hormone therapy, highlighting its benefits when started early, particularly for women with low cardiovascular risk. It stresses the importance of individualized care and decision-making when considering HT for managing menopausal symptoms.