Abstract
Allergic bronchopulmonary aspergillosis (ABPA) is characterized by an early allergic response and late-phase lung injury in response to repeated exposure to Aspergillus antigens, as a consequence of persistent fungal colonization of the airways. Here, we summarize the clinical and pathological features of ABPA, focusing on thick mucus plugging, a key observation in ABPA. Recent findings have indicated that luminal eosinophils undergo cytolytic extracellular trap cell death (ETosis) and release filamentous chromatin fibers (extracellular traps, ETs) by direct interaction with Aspergillus fumigatus. Production of ETs is considered to be an innate immune response against non-phagocytable pathogens using a “trap and kill” mechanism, although eosinophil ETs do not promote A. fumigatus damage or killing. Compared with neutrophils, eosinophil ETs are composed of stable and condensed chromatin fibers and thus might contribute to the higher viscosity of eosinophilic mucus. The major fate of massively accumulated eosinophils in the airways is ETosis, which potentially induces the release of toxic granule proteins and damage-associated molecular patterns, epithelial damage, and further decreases mucus clearance. This new perspective on ABPA as a luminal hypereosinophilic disease with ETosis/ETs could provide a better understanding of airway mucus plugging and contribute to future therapeutic strategies for this challenging disease.
Highlights
Allergic bronchopulmonary aspergillosis (ABPA) is a disease entity first proposed by Hinson and colleagues as bronchopulmonary aspergillosis in 1952 [1]
It is characterized by peripheral blood eosinophilia, increased levels of serum IgE, an immediate skin reaction and/or specific IgE/IgG antibodies to Aspergillus fumigatus due to type I and III hypersensitivity reactions, and ABPA-Luminal Hypereosinophilia With extracellular trap cell death (ETosis) radiographic findings including pulmonary opacities, central bronchiectasis, and mucus plugs [3,4,5]
Considerable evidence has indicated the close association between the sputum eosinophil count and/or the eosinophil granule protein concentration and asthma severity [8, 9], much less attention has been paid to luminal eosinophils in ABPA
Summary
Allergic bronchopulmonary aspergillosis (ABPA) is a disease entity first proposed by Hinson and colleagues as bronchopulmonary aspergillosis in 1952 [1]. “The investigation of the resected lungs of ABPM patients revealed the airway walls plugged by AMwF were invaded with eosinophils and small round cells including plasma cells and were ulcerated, resulting in eosinophilic infiltration into the allergic mucin. Our recent studies indicated eosinophil cell-death mediated degranulation, i.e., eosinophil ETosis, which might play an important role in the generation of mucus plugs [39, 40].
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