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Neutrophils and extracellular traps in crystal-associated diseases

Trends in Molecular Medicine 2024 13 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Qiuyue Ma, Qiuyue Ma, Stefanie Steiger

Summary

Researchers reviewed how crystals that form inside the body — such as uric acid crystals in gout or silica particles in silicosis — trigger immune cells called neutrophils to release web-like DNA traps (NETs) that cause tissue damage. This inflammatory mechanism may also be relevant to how hard microplastic particles behave once inside human tissues, as they share some physical properties with disease-causing crystals.

Crystalline material can cause a multitude of acute and chronic inflammatory diseases, such as gouty arthritis, silicosis, kidney disease, and atherosclerosis. Crystals of various types are thought to cause similar inflammatory responses, including the release of proinflammatory mediators and formation of neutrophil extracellular traps (NETs), processes that further promote necroinflammation and tissue damage. It has become apparent that the intensity of inflammation and the related mechanisms of NET formation and neutrophil death in crystal-associated diseases can vary depending on the crystal type, amount, and site of deposition. This review details new mechanistic insights into crystal biology, highlights the differential effects of various crystals on neutrophils and extracellular trap (ET) formation, and discusses treatment strategies and potential future approaches for crystal-associated disorders.

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