Does <scp>ABPA</scp> Contribute to Bronchiectasis? A Structured Evaluation of Competing Hypotheses

Whether allergic bronchopulmonary aspergillosis (ABPA) causes bronchiectasis or merely represents Aspergillus fumigatus colonisation of damaged airways remains debated. Establishing causality is challenging because airway damage is predominantly driven by host immune responses rather than by direct fungal invasion. We systematically evaluate four competing hypotheses: (i) ABPA causes bronchiectasis, (ii) reverse causation, with bronchiectasis predisposing to ABPA, (iii) a shared underlying factor independently producing both conditions and (iv) a spurious association. We evaluate radiological, pathological, immunological, temporal and therapeutic evidence in relation to these hypotheses. The characteristic radiological phenotype (central bronchiectasis and high-attenuation mucus), eosinophil-dominant histopathology and disease-specific immunological profile (typically absent in other forms of bronchiectasis despite Aspergillus colonisation) distinguish ABPA from incidental colonisation. Randomised controlled trials demonstrating that antifungal treatment or anti-inflammatory therapy (glucocorticoids and biological agents) improve clinical and immunological outcomes argue against a purely spurious association. Temporal observations indicate that ABPA precedes bronchiectasis in many cases. While uncertainty remains and host susceptibility is likely essential, the available evidence suggests that ABPA contributes to bronchiectasis through antigen-driven immune injury, supporting the use of appropriate antifungal and immunomodulatory therapy in selected patients.