ReviewFrontiers in allergy2026
Fibroblast-centered mechanisms of chronic inflammation and airway remodeling in allergic bronchopulmonary aspergillosis.
Review in Frontiers in allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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10 authors.
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Abstract
Allergic bronchopulmonary aspergillosis (ABPA) is a complex hypersensitivity lung disease driven predominantly by type 2 immune responses. However, the classical immunological paradigm fails to adequately explain the persistent airway structural damage and frequent relapses observed even after inflammatory control is achieved. This review proposes a fibroblast-centered mechanistic framework that synthesizes evidence from ABPA, fungal-associated airway diseases, and pulmonary fibrosis to systematically delineate the mechanisms linking fibroblasts to chronic inflammation and airway remodeling. In the context of chronic inflammation and persistent epithelial injury, fibroblasts can be activated by various signals, including type 2 cytokines such as interleukin-4 (IL-4) and IL-13. Upon activation, fibroblasts exert their effects through functionally distinct subpopulations: they actively recruit eosinophils through chemokine secretion (e.g., CCL11), establishing a positive feedback loop of "epithelial injury-fibroblast activation-eosinophil infiltration-tissue damage" that sustains and amplifies inflammation. Prolonged activation further drives fibroblast-to-myofibroblast transition, characterized by expression of
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