Persistent desmoglein-1 downregulation and periostin accumulation in histologic remission of eosinophilic esophagitis

[Display omitted] Patients with eosinophilic esophagitis (EoE) require long-lasting resolution of inflammation to prevent fibrostenosis and dysphagia. However, the dissociation between symptoms and histologic improvement suggests persistent molecular drivers despite histologic remission. We characterized persisting molecular alterations in pediatric patients with EoE using tissue transcriptomics and proteomics. Esophageal biopsy samples (n = 247) collected prospectively during 189 endoscopies from pediatric patients with EoE (n = 36, up to 11 follow-up endoscopies) and pediatric controls (n = 44, single endoscopies) were subjected to bulk transcriptomics (n = 96) and proteomics (n = 151). Intercellular junctions (desmoglein-1/3, desmoplakin, E-cadherin) and epithelial-to-mesenchymal transition (vimentin:E-cadherin ratio) were assessed by immunofluorescence staining. Active EoE (≥15 eosinophils per high-power field [eos/hpf]), inactive EoE (