Bronchiectasis has traditionally been characterized as a predominantly neutrophil-driven airway disease. Recent work, summarized in this review, highlights a distinct subset of patients with bronchiectasis who demonstrate eosinophilic airway inflammation. The authors aim to summarize emerging evidence on the pathogenesis, clinical relevance, and therapeutic implications of this eosinophilic endotype and to consider how it may inform a more personalized approach to management.
Eosinophilic bronchiectasis is recognized using measurements of blood or sputum eosinophils. The review emphasizes that while these markers are used in clinical and research settings, the optimal biomarker strategy and the most appropriate numerical thresholds have not been established. As a result, definitions vary between studies, which complicates comparisons and clinical decision-making. The authors note a need to standardize biomarker selection and threshold values to reliably identify the eosinophilic endotype.
Eosinophilic inflammation in bronchiectasis is not isolated; it frequently coexists with or overlaps other type 2 airway conditions. The review lists asthma, allergic bronchopulmonary aspergillosis (ABPA), and cystic fibrosis as disease states in which type 2 immune activation and eosinophilia are observed. These overlapping states make clinical interpretation more complex because eosinophilia may reflect primary bronchiectasis inflammation, comorbid type 2 disease, or both. Despite this complexity, eosinophilic inflammation may carry implications for disease severity and prognosis, suggesting that recognizing this endotype could be clinically informative.
Therapeutic data specific to eosinophilic bronchiectasis are limited and mainly observational. The review highlights two treatment domains where eosinophilia may be clinically actionable:
Inhaled corticosteroids (ICS): Observational evidence suggests that patients with higher eosinophil counts may derive greater benefit from inhaled corticosteroids. The authors indicate this as a potential avenue for treatment selection, but they also stress that evidence is not definitive and that a standardized biomarker-based approach to guide ICS use is lacking.
Biologic therapies: Early, primarily preliminary studies of biologics—targeted agents used in type 2 airway inflammation—are described as promising, particularly in patients with concurrent ABPA or asthma. However, the review clearly states that the benefit of biologic agents for eosinophilic bronchiectasis independent of overlapping type 2 conditions remains uncertain because randomized and robust trial data are not yet available.
The body of evidence reviewed is constrained by the predominance of observational studies and heterogeneous definitions of eosinophilia. The review notes that much of the therapeutic signal for ICS and biologics comes from non-randomized data or early-phase studies, limiting the ability to draw firm conclusions about efficacy and appropriate patient selection. The authors call attention to the need for higher-quality trials and for consistent use of biomarkers across studies.
The review outlines key priorities for future research in eosinophilic bronchiectasis:
Eosinophilic bronchiectasis represents a distinct inflammatory endotype within the broader bronchiectasis population that may allow a more personalized management approach. Current evidence suggests potential responsiveness to inhaled corticosteroids and possible utility of biologic therapies in selected patients, especially those with overlapping ABPA or asthma, but data are largely observational. The review concludes that standardizing biomarker definitions and conducting rigorous trials are necessary next steps to clarify prognosis and to guide targeted therapies in this group.
Note: Details on specific biomarker thresholds, quantitative outcomes, or randomized trial results were not reported in the source abstract and therefore are not included here.