Eosinophils in bronchiectasis
PURPOSE OF REVIEW: Bronchiectasis has traditionally been viewed as a predominantly neutrophil-driven airway disease. Recognition of eosinophilic inflammation in a substantial subset of patients has challenged this paradigm. This review summarizes emerging evidence regarding its pathogenesis, clinical significance, and therapeutic implications. RECENT FINDINGS: Eosinophilic bronchiectasis is identified using blood or sputum eosinophilia, although optimal biomarkers and thresholds are unclear. Eosinophilic inflammation occurs in bronchiectasis and overlapping disease states characterized by type 2 immune activation, including asthma, allergic bronchopulmonary aspergillosis, and cystic fibrosis, complicating diagnosis but potentially informing disease severity, prognosis, and treatment options. Evidence for targeted therapies is limited to largely observational data. Patients with elevated eosinophil counts may derive greater benefit from inhaled corticosteroids. Early studies of biologics appear promising, particularly in patients with coexisting ABPA or asthma, although their benefit in eosinophilic bronchiectasis independent of these conditions remains uncertain. SUMMARY: Eosinophilic bronchiectasis represents a distinct inflammatory endotype that may enable a more personalized approach to disease management. Future studies should identify clinically relevant biomarkers to standardize its definition, clarify its relationship with overlapping type 2 airway diseases, and guide the use of inhaled corticosteroids and biologics.
Authors
- Megan Trieu (ORCID: https://orcid.org/0009-0005-8739-0893)
- Praveen Akuthota (ORCID: https://orcid.org/0000-0001-6655-7520)
- Jeffrey Barry
Institutions
- University of California System (US)
- University of California San Diego (US)
Publication Details
- Journal
- Current Opinion in Pulmonary Medicine
- Published
- 2026-09-18
- DOI
- https://doi.org/10.1097/mcp.0000000000001315
- Primary Topic
- Cystic Fibrosis Research Advances
- Type
- article
- Field-Weighted Citation Impact
- 0.00