This in vitro study examined how timing of dupilumab treatment (early = concurrent with IL-13 vs. delayed = 4 days after IL-13) affects restoration of airway epithelial barrier function in primary human bronchial epithelial cells grown at air-liquid interface, using TEER, permeability assays, immunofluorescence, and single-cell RNA sequencing.
Early dupilumab preserved transepithelial electrical resistance (TEER) and reduced permeability, while delayed dupilumab yielded only partial TEER recovery with persistently increased permeability; TEER inversely correlated with MUC5AC expression, and asthmatic epithelium showed disrupted occludin localization around goblet cells.
Findings are from an in vitro air-liquid interface model only — no in vivo or clinical validation; the study does not include patient-level outcome data to directly link cellular findings to variable clinical responses; sample size and donor characteristics for primary bronchial cells are not specified in the abstract.
This mechanistic work suggests that earlier initiation of dupilumab in asthma may better preserve airway barrier integrity by preventing goblet cell-driven remodeling, while delayed treatment leaves residual permeability defects. Clinicians should consider that patients starting dupilumab after established airway remodeling may experience incomplete epithelial recovery.
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