Karen Pendergrass, Standards Team

This study characterized the siderophores produced by Microsporum and Trichophyton species, revealing that M. canis secretes ferrichrome and ferricrocin under iron-limited conditions, indicating siderophore pathways as exploitable therapeutic targets.

Short-chain fatty acids are microbially derived metabolites that regulate epithelial integrity, immune signaling, and microbial ecology. Their production patterns and mechanistic roles provide essential functional markers within microbiome signatures and support the interpretation of MBTIs, MMAs, and systems-level microbial shifts across clinical conditions.

Microbial Metallomics is the study of how microorganisms acquire, use, regulate, and transform metals in any biological or environmental context.

Escherichia coli (E. coli) is a versatile bacterium, from gut commensal to pathogen, linked to chronic conditions like endometriosis.

This review synthesizes evidence on melatonin’s effects on skeletal muscle health, exercise, and the gut–muscle axis, highlighting its mitochondrial, anti-inflammatory, and microbiome-modulating actions, with emphasis on microbial associations relevant to muscle aging and performance.

A single dose of melatonin enhances growth hormone secretion and reduces somatostatin in resistance-trained young males, especially when combined with heavy exercise, but has less effect in females. IGF-1 levels remain unchanged. Melatonin is safe acutely at these doses.

Dementia with Lewy bodies (DLB) brains show widespread copper depletion and region-specific sodium, manganese, iron, and selenium alterations. While copper loss is common to AD and PDD, DLB presents a distinct metallomic fingerprint, enabling disease differentiation via PCA. Metallomic profiling may aid in diagnosing overlapping dementias and reveals unique pathophysiological signatures.

Urease is a nickel-dependent microbial enzyme that breaks down urea into ammonia, altering local pH and nitrogen availability. While essential for microbial survival in acidic niches and nutrient-limited environments, urease activity also contributes to conditions like ulcers, urinary stones, colitis, and hepatic encephalopathy.

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.

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.

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.

Nickel allergic contact mucositis was identified in over 90% of endometriosis patients with IBS-like symptoms. A low-nickel diet significantly reduced gastrointestinal, extra-intestinal, and gynecological symptoms, revealing nickel sensitivity as a key driver of endometriosis symptomatology.

Iron supplementation in infants reduces Bifidobacterium abundance by 6.37%, as confirmed by meta-analysis. While critical for anemia prevention, oral iron may disrupt the infant gut microbiota, potentially supporting pathogen growth. Prebiotic co-administration could mitigate adverse effects.

OverviewIron is a pivotal nutrient at the host–pathogen interface. Virtually all microbes (with rare exceptions like Borrelia) require iron for processes from DNA synthesis to respiration. [1] In human hosts, free iron is vanishingly scarce due to “nutritional immunity,” wherein iron is locked up in hemoproteins or tightly bound by transport proteins.[2] This metal tug-of-war […]

High-dose enteral iron supplementation in VLBW infants was associated with reduced microbial diversity, Proteus enrichment, and increased microbial potential for ferroptosis and epithelial invasion, highlighting risks of intestinal dysbiosis.

This review outlines current strategies targeting siderophore biosynthesis as a therapeutic approach to microbial infections, emphasizing enzyme-specific inhibitors, nanoparticle delivery, and CRISPR-based interventions to impair iron acquisition and reduce virulence.

This review outlines how Staphylococcus aureus overcomes host nutritional immunity by acquiring iron, manganese, and zinc, underscoring the critical role of metal transport systems in virulence and immune evasion.

Siderophores are microbial iron-chelating molecules that enable pathogens to overcome host iron restriction, shape microbiome ecology, and serve as therapeutic targets.

This review details recent enzymatic and structural insights into NRPS-dependent and NRPS-independent siderophore biosynthesis, emphasizing implications for antimicrobial development and microbiome-targeted therapies.

Nutritional immunity restricts metal access to pathogens, leveraging sequestration, transport, and toxicity to control infections and immunity.

Redundant siderophores and an Sst catechol transporter enable Staphylococcus aureus iron acquisition from transferrin, including catecholamine-liberated and xenosiderophore-bound pools, and jointly drive virulence in mice. Targeting Hts, Sir, and Sst impairs growth and organ colonization.

XusB in Bacteroides thetaiotaomicron binds enterobactin in OMVs, sustains commensal fitness, and creates a lipocalin 2 resistant iron pool that Salmonella can recapture, redefining commensal-iron-acquisition-and-nutritional-immunity during colitis.

Aferric enterobactin disables myeloperoxidase, granting E. coli a survival edge in colitis, while lipocalin 2 restores enzyme function and counters colonization.

Lipocalin 2 sequesters enterobactin to starve bacteria of iron, while the iroA cluster glucosylates enterobactin into salmochelins that evade capture, sustaining virulence. Targeting iroA may restore host iron withholding without disrupting commensals.