Type 2 Inflammation in Airway Diseases: Eosinophilic Bronchiectasis as an Emerging Phenotype

Bronchiectasis is a chronic and highly heterogeneous airway disease traditionally regarded as a neutrophil-dominated condition driven by persistent infection and dysregulated innate immunity. Over the last decade, this traditional view has been increasingly challenged by the identification of distinct inflammatory phenotypes with important biological and therapeutic implications.Among these, eosinophilic bronchiectasis has emerged as a clinically meaningful and mechanistically distinct phenotype, characterized by type 2 (T2) immune activation, eosinophil-driven airway inflammation, and differential responsiveness to targeted therapies.In this narrative review, we provide an overview of eosinophilic bronchiectasis, emphasizing epidemiology, immunopathogenesis, and cellular and molecular mechanisms underlying airway damage and remodelling. We discuss key pathways involving eosinophils, epithelial-immune interactions, and T2 cytokine signalling, as well as established and emerging biomarkers for phenotype identification.We proposed a diagnostic framework and definitions for eosinophilic bronchiectasis, i.e. definite (airway eosinophilia with sputum or bronchoalveolar lavage eosinophils ≥ 3%), probable (persistent peripheral blood eosinophilia ≥ 300 cells/µL), and possible (a single elevated blood eosinophil count of ≥ 150-300 cells/µL or elevated FeNO > 25 ppb in the absence of asthma), to be provisionally used in the absence of shared consensus criteria.Particular attention is devoted to therapeutic implications, including biologic agents targeting the IL-5/IL-5r axes and novel disease-modifying strategies for eosinophilic disorders. Finally, we highlight unmet needs and future research directions toward precision medicine approaches aimed at improving outcomes in this increasingly recognized bronchiectasis phenotype.