Karen Pendergrass, Standards Team

Mendelian‑randomization of Japanese WAS data shows a bidirectional genetic link between Graves’ disease and rheumatoid arthritis. The findings reinforce shared autoimmune pathways, highlight overlapping Prevotella‑dominant gut dysbiosis, and support reciprocal clinical screening and microbiome‑targeted interventions.

Graves Disease potentiates depression via autoimmune cytokines, hormonal excess and gut‑microbiome shifts. This review consolidates epidemiology and mechanisms, highlighting microbial signatures (Prevotellaceae, CFA depletion) of translational interest.

Mendelian-randomization of Asian WAS data shows Crohn disease genetics raise Graves disease risk, while ulcerative colitis genetics are protective, highlighting microbiome-immune pathways linking gut and thyroid autoimmunity.

This bidirectional Mendelian Randomization (R) study establishes a causal link between Graves’ disease and gut microbiome alterations, confirming thyroid–gut axis interactions and identifying key microbial taxa as risk or protective factors.

This review maps the bidirectional interactions between toxic and essential metals and the gut microbiota, detailing microbial shifts and host impacts. It highlights specific microbial taxa disrupted by metals like arsenic, cadmium, and nickel, providing insight into metal-driven dysbiosis and its implications for disease pathogenesis.

This study shows that Staphylococcus aureus uses ABC and H transporters to overcome host-imposed manganese starvation via calprotectin, preserving OD activity and enabling systemic infection.

This review highlights Staphylococcus aureus as a multifaceted pathogen with niche-specific colonization, immune evasion, iron acquisition strategies, and extensive resistance mechanisms, emphasizing its microbiome interactions and emerging therapeutic targets.

This review examines bacterial resistance systems to toxic metals, detailing efflux pumps, TPases, and metallothioneins. It explores their mechanisms, gene regulation, and clinical or environmental relevance.

This review outlines how S. aureus leverages diverse virulence factors—α-toxin, leukocidins, biofilms, and immune evasion mechanisms—regulated by systems like Agr to persist and cause disease. It discusses anti-virulence strategies and implications for targeted therapies.

Metallophores in S. aureus enable metal acquisition and virulence; disrupting these systems may offer novel antimicrobial strategies.