Divine Aleru, Microbiome Signatures Research Coordinator

This study shows that the Salmonella peptide MgtR directly limits the MgtA magnesium transporter during Mg2+ starvation. Deleting mgtR raises MgtA protein levels and makes MgtA appear earlier, which improves growth in low magnesium when other transporters are absent.

This study shows that the magnesium transporter MgtE suppresses Pseudomonas aeruginosa type III secretion by blocking ExsA translation. MgtE activates the GacAS system, increases rsmY and rsmZ, and limits ExsA production, which lowers T3SS gene transcription without reducing exsA mRNA.

What was studied? This experimental study investigated how the bacterial magnesium transporter A (MgtA) functions at the biochemical level and how membrane lipids and free magnesium concentrations regulate its activity. The authors focused on MgtA from Escherichia coli as a model system to clarify how this transporter responds to magnesium limitation and how it integrates […]

This review explains how hosts restrict pathogens by triggering magnesium limitation signals during infection. It shows that bacteria respond to what they feel inside their cytoplasm and highlights Salmonella’s need for Mg2+ transport systems and stress sensors to survive inside macrophages.

This review explains that the small intestine absorbs magnesium through regulated transcellular and paracellular pathways. Hormones, luminal pH sensing, and proton pump inhibitors can suppress absorption, while fermentation-linked acidification may support uptake. It links dysbiosis and inflammation to impaired magnesium bioavailability.

This review explains how magnesium imbalance affects neuromuscular and cardiac function and why lab results can mislead. It highlights pre-analytical errors, limits of serum magnesium, and strong links between magnesium, potassium, calcium, and gut-related absorption or loss.

This mini-review explains how higher-dose magnesium can reduce bacterial adhesion and weaken biofilm formation. It highlights why biofilms resist cleaning and heat, and it summarizes evidence that magnesium in milk can reduce Bacillus biofilms and lower survival after pasteurization.

This study shows that low gut magnesium activates a virulence pathway in EHEC O157:H7 that boosts LEE gene expression and intestinal attachment. A magnesium-rich diet raised colon magnesium and sharply reduced bacterial adherence in mice, supporting magnesium as an anti-virulence approach.

This review explains how magnesium, zinc, copper, iron, and selenium shape innate and adaptive immunity and long-term inflammation. It highlights that magnesium deficiency can weaken the gut barrier and reduce bifidobacteria, which can raise inflammatory cytokines and worsen immune balance.

This review explains how bacteria sense magnesium outside and inside the cell, switch among Mg2+ transporters, and remodel their envelope to survive low Mg2+. It shows how Mg2+ limitation and host stresses can activate virulence programs, especially in Salmonella and related pathogens.

This review explains how magnesium supports energy, vascular tone, glucose handling, bone strength, and brain excitability, and why low intake or poor absorption can raise chronic disease risk. It also clarifies why serum magnesium can miss deficiency and why gut factors matter for magnesium availability.

This review explains how magnesium supports energy, vascular function, immunity, glucose control, bone strength, and muscle health, and how low intake or poor absorption can raise risks for cardiometabolic disease and inflammation. It also highlights gut factors that may reduce magnesium availability.

Mercury primarily affects microbiome pathogenesis by acting as a strong toxic selector that enriches organisms carrying mercury detox systems and the mobile elements that often co-carry antimicrobial resistance. In the gut, mercury speciation and bioavailability are shaped by thiols and sulfide chemistry, while microbial responses are dominated by the mer operon toolkit that detects Hg(II), traffics it intracellularly, and reduces it to Hg(0) for detox and loss from the cell.

This review explains how dietary pectin may shift gut microbiota and SCFA production to shape allergy risk, while also noting reports of pectin-related sensitization and anaphylaxis. It highlights structure-dependent microbial associations and immune pathways that matter in asthma and food allergy.

This review explains how thiol-based chelators bind mercury, cadmium, and lead and how that chemistry guides clinical treatment. It compares common agents such as DMSA and DMPS, outlines safety tradeoffs, and clarifies why brain and intracellular metal stores remain hard to remove.

This study shows the gut microbiome helps clear dietary methylmercury by demethylating it in the intestine. People differed widely in elimination rates, which tracked with stool demethylation activity and specific taxa patterns, especially Alistipes.

This pilot study in late pregnancy linked maternal gut microbiota to mercury biomarkers and tested whether microbes directly change stool methylmercury. Stool methylmercury did not predict fetal exposure, and mercury cycling genes were largely absent, suggesting indirect microbiome pathways may matter more.

This review explains how mercury form and exposure route change diagnosis and treatment. It compares blood, urine, and hair biomarkers, discusses why symptoms do not always match measured levels, and summarizes supportive care and chelation options while noting that firm treatment thresholds remain hard to define.

This review explains how workplace microbes, chemicals, metals, and air pollution can change the adult human microbiome. It highlights links to colonization, gut permeability, and immune effects, and it suggests that stopping exposure alone may not reverse risk if microbiome changes persist.

Mercury pollution reshaped a soil microbiome by lowering alpha diversity and increasing between-community divergence. A focal Pseudomonas strain survived mercury stress by acquiring mercury resistance, and conjugative elements spread merA widely across taxa, showing how toxicants can drive community change and resistance gene flow.

This study shows human gut microbiota can demethylate methylmercury and that detox rates vary by exposure level and food source. Higher Desulfovibrio and methanogen signals aligned with faster demethylation, while mer and hgcAB genes did not explain the process.

Mercury-contaminated paddy soil increased plant and human pathogen signals under both ambient and elevated CO₂. Metagenomics showed strong activation of efflux pumps, especially the RND family, alongside higher adherence and secretion-related virulence factors, linking metal exposure to antibiotic resistance potential and pathogen aggressiveness.

This study shows that trace mercury exposure can favor the USA300-LV MRSA lineage in South America. Mercury reverses the fitness cost of COMER, helps USA300-LV outcompete other strains, and increases expression of major virulence genes under sub-inhibitory mercury.

This review explains how methylmercury forms in the environment, enters the body, and reaches the brain through fast “exchange” chemistry with sulfur and selenium groups. It highlights microbial methylation as the exposure driver and selenoenzymes as vulnerable targets that amplify neurotoxicity.