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Allergic bronchopulmonary aspergillosis (ABPA) is a pulmonary disorder caused by exaggerated hypersensitivity to Aspergillus species, namely Aspergillus fumigatus. It is characterized by poorly controlled asthma, recurrent pulmonary infiltrates, and bronchiectasis often with thick, viscous eosinophilic mucus plugging.1 Although the mechanism of this hyperdense mucus generation is poorly understood, the severity of this mucus plugging, which may represent severe inflammation, is associated with recurrent relapse.2 Extracellular trap cell death (ETosis) of human leucocytes, particularly neutrophils and eosinophils, is a distinct programmed cell death pathway.3 It is characterized by release of filamentous chromatin structures (DNA traps) in contrast to cell apoptosis.4 DNA trap formation is considered to be an innate immune reaction by ensnaring microorganisms, although its excess production could be pathogenic.5 For instance, in thick and viscous airway fluids from patients with cystic fibrosis, large numbers neutrophil-derived DNA traps are present (also called neutrophil extracellular traps; NETs).4,5 Notably, treatment by inhalation of recombinant human DNase improved lung function,6 indicating the pathogenicity of NETs. In contrast, the clinical significance of eosinophil ETosis-derived DNA traps is less well studied. We recently revealed their involvement in high viscosity of sinus secretions, a characteristic in refractory eosinophilic chronic rhinosinusitis (ECRS) and eosinophilic otitis media (EOM).4 Here, we report a case of ABPA, which had bronchiectasis with viscous mucus plugging containing abundant DNA traps. The patient demonstrated a rapid clinical response and decrease in DNA traps to systemic corticosteroid. A 64-year-old Japanese man was referred to our hospital for cough, sputum, and chest pain. He had a 10-year history of asthma and had experienced the above symptoms for 6 months before admission. Laboratory examination revealed an elevated blood eosinophil count (WBC: 6800/mL, eosinophil: 1120/mL) and serum total IgE (1628 IU/mL). Testing for specific IgE and precipitating antibodies against A. fumigatus was positive. Chest X-ray and computed tomography (CT) revealed infiltration with bronchial wall thickening, central bronchiectasis, and mucoid impaction with middle and lower lobe predominance. Pulmonary function testing showed reduced forced expiratory volume in 1 s and a force vital capacity ratio (FEV1/FVC) of 67.9%. From these findings, he was diagnosed with ABPA, fulfilling the diagnosis criteria1. He was

Mucus plugging in allergic bronchopulmonary aspergillosis: Implication of the eosinophil DNA traps