IL-33 Drives Inflammatory Changes and Extracellular Trap Formation in Eosinophils Involving Oxidised LDL and Complement Pathways - PubMed
5 hours ago
- #IL-33
- #ETosis
- #eosinophils
- IL-33 levels are elevated in eosinophilic diseases and upregulate IL-33 receptor expression on eosinophils in type 2-high environments.
- IL-33 and TNF-α induce an inflammatory gene signature in eosinophils, upregulating cell surface markers (oxLDL receptor 1, CD22, CD4, ICAM-1) and inflammatory mediators (C3, CCL3/4, IL1A/B).
- Eosinophils from nasal polyps show a gene expression profile similar to IL-33-stimulated eosinophils.
- OxLDL and complement fragments prolong eosinophil survival and alter adhesion molecule expression.
- IL-33 triggers ETosis via NADPH oxidase, MAPK, and PI3K pathways.
- IL-33, oxLDL, and complement pathways induce inflammatory changes in eosinophils, promoting an ETosis-prone phenotype, suggesting potential therapeutic targets for eosinophilic diseases.