ReviewFrontiers in medicine2026
Eosinophilic and type 2 inflammation in bronchiectasis: from phenotype recognition toward endotype-informed therapy.
Review in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors.
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Abstract
Bronchiectasis is increasingly recognized as biologically heterogeneous, yet the clinical meaning of eosinophilic and type 2 (T2)-associated signals remains uncertain. This review reassesses whether the field has progressed from recognition of an eosinophilic phenotype to a bronchiectasis-specific, therapeutically actionable T2 endotype. Blood eosinophil count (BEC), airway eosinophilia, fractional exhaled nitric oxide, total immunoglobulin E, and pathway-level signatures capture overlapping but non-equivalent features. Current evidence supports an eosinophilic phenotype more strongly than a unified bronchiectasis-specific T2 endotype. Airway studies confirm eosinophil activation in selected patients, but direct evidence for a complete and reproducible epithelial alarmin-T2-cell-IL-4/IL-5/IL-13 pathway is limited, and asthma, allergic bronchopulmonary aspergillosis, fungal sensitization, chronic rhinosinusitis, and chronic obstructive pulmonary disease can confound biomarker interpretation. Prognostic associations are non-linear and context dependent: persistent or high eosinophilia and very low BEC have each been associated with adverse outcomes in different settings. Inhaled corticosteroids show biological effects and exploratory eosinophil-associated response signals, but these do not validate BEC as a predictive biomarker or support treatment solely for elevated BEC. In MAHALE, benralizumab produced profound eosinophil depletion without demonstrated clinical efficacy in the population studied; severe under-recruitment and limited eosinophilic enrichment restrict inference for persistently eosinophilic disease. Evidence from biologic-treated severe asthma with coexisting bronchiectasis remains indirect for bronchiectasis efficacy. The review therefore defines the validation pathway required before phenotype recognition can inform treatment selection: repeated stable-state phenotyping, airway biological validation, separation from T2 comorbidities, prespecified treatment-by-biomarker interaction analyses, and adequately powered biomarker-enriched trials.
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