ArticleFrontiers in immunology2019
Reduced Neutrophil Extracellular Trap (NET) Formation During Systemic Inflammation in Mice With Menkes Disease and Wilson Disease: Copper Requirement for NET Release.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- The role of metal ions iron, copper, and zinc in the immune microenvironment of gastric cancer.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- ATP7B-maintained copper stores in myeloid progenitors are required for functional maturation of neutrophils.Cell reports · 2026Article
- Cuproptosis in Sepsis: Cell Type-Specific Mechanisms and Clinical Prospects.Drug design, development and therapy · 2026Review
- The gut-liver-kidney-brain axis in Wilson disease: copper speciation-flux and barrier-mediated organ crosstalk.Frontiers in immunology · 2026Review
- Article
- Non-classical neutrophil extracellular traps induced by PAR2-signaling proteases.Cell death & disease · 2025Article
- Neutrophil extracellular traps in ischemic stroke: mechanisms, clinical implications, and therapeutic potential.Frontiers in neurology · 2025Review
- Editorial: Community series in intravital microscopy imaging of leukocytes, volume II.Frontiers in immunology · 2025Article
- Neutrophil extracellular traps in diseases of the female reproductive organs.Frontiers in immunology · 2025Review
- Skin repair and infection control in diabetic, obese mice using bioactive laser-activated sealants.Biomaterials · 2024Article
- Immune remodulation in pediatric inherited metabolic liver diseases.World journal of hepatology · 2024Review
- How metals fuel fungal virulence, yet promote anti-fungal immunity.Disease models & mechanisms · 2023Review
- The emerging role of neutrophil extracellular traps in endometritis.Frontiers in immunology · 2023Review
- Neutrophil degranulation and severely impaired extracellular trap formation at the basis of susceptibility to infections of hemodialysis patients.BMC medicine · 2022Article
- Neutrophil extracellular traps participate in the development of cancer-associated thrombosis in patients with gastric cancer.World journal of gastroenterology · 2022Article
- Gut-derived lipopolysaccharide promotes alcoholic hepatosteatosis and subsequent hepatocellular carcinoma by stimulating neutrophil extracellular traps through toll-like receptor 4.Clinical and molecular hepatology · 2022Article
- Acclimation to Nutritional Immunity and Metal Intoxication Requires Zinc, Manganese, and Copper Homeostasis in the PathogenicFrontiers in cellular and infection microbiology · 2022Review
- Nutritional immunity: the impact of metals on lung immune cells and the airway microbiome during chronic respiratory disease.Respiratory research · 2021Review
- Article
- On Neutrophil Extracellular Trap (NET) Removal: What We Know Thus Far and Why So Little.Cells · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophil extracellular traps (NETs) contribute to pathological disorders, and their release was directly linked to numerous diseases. With intravital microscopy (IVM), we showed previously that NETs also contribute to the pathology of systemic inflammation and are strongly deposited in liver sinusoids. Over a decade since NET discovery, still not much is known about the metabolic or microenvironmental aspects of their formation. Copper is a vital trace element essential for many biological processes, albeit its excess is potentially cytotoxic; thus, copper levels are tightly controlled by factors such as copper transporting ATPases, ATP7A, and ATP7B. By employing IVM, we studied the impact of copper on NET formation during endotoxemia in liver vasculature on two mice models of copper excess or deficiency, Wilson (ATP7B mutants) and Menkes (ATP7A mutants) diseases, respectively. Here, we show that respective ATP7 mutations lead to diminished NET release during systemic inflammation despite unaltered intrinsic capacity of neutrophils to cast NETs as tested
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