Eosinophil Extracellular Traps in Health and Disease: From Host Defense to Chronic Inflammation

Eosinophils are tissue-adapted granulocytes with important roles in host defense, immune regulation, barrier responses, and inflammatory disease. Beyond classical degranulation, activated eosinophils can release eosinophil extracellular traps (EETs), extracellular DNA and protein structures that arise through cytolytic nuclear EETosis or rapid mitochondrial DNA (mtDNA) release. These traps may contribute to host protection by immobilizing pathogens and concentrating eosinophil granule proteins at sites of mucosal or tissue inflammation. However, when EET formation is excessive, persistent, or insufficiently cleared, the same structures may promote epithelial injury, mucus viscosity, thromboinflammation, tissue remodeling, fibrosis, and chronic eosinophilic inflammation. This review summarizes the cellular mechanisms, structural organization, inducing stimuli, and disease relevance of EETs. Particular attention is given to infectious settings, eosinophilic airway and middle-ear disease, systemic vasculitic and hypereosinophilic disorders, inflammatory skin and ocular diseases, eosinophilic gastrointestinal disease, and cancer. Current evidence indicates that EETs should be interpreted as context-dependent eosinophil effector structures with dual biological potential. Although their mechanistic relevance is increasingly recognized, further histological, functional, and clinical validation is needed before EETs can be established as reliable biomarkers or therapeutic targets.