{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T10:00:45Z","timestamp":1790848845230,"version":"4.1.0"},"reference-count":87,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Med."],"abstract":"<jats:p>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\u2013T2-cell\u2013IL-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.<\/jats:p>","DOI":"10.3389\/fmed.2026.1987219","type":"journal-article","created":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T09:52:43Z","timestamp":1790848363000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Eosinophilic and type 2 inflammation in bronchiectasis: from phenotype recognition toward endotype-informed therapy"],"prefix":"10.3389","volume":"13","author":[{"given":"Luwen","family":"Liang","sequence":"first","affiliation":[{"name":"Department of General Practice, The First Affiliated Hospital of Gannan Medical University","place":["Ganzhou, 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