Epithelial Barrier Dysfunction Module

A conserved cross-tissue pathophysiology module for the "epithelial barrier hypothesis" of allergic / type 2 inflammatory disease. Epithelial barriers of the skin, airway, gut, and esophagus share critical functions (a physical junctional barrier plus innate immune defense), and in allergic patients — regardless of tissue location — barrier homeostasis is skewed toward loss of terminal differentiation, reduced junctional integrity, and impaired innate defense. The conserved sequence is: an epithelial barrier insult or intrinsic junctional/differentiation defect disrupts the barrier; increased transepithelial allergen and microbial penetration activates innate immunity and antigen-presenting cells; a type 2 (TH2) milieu drives IgE class switch and allergic sensitization; and allergic disease is initiated at the affected barrier and, beyond it, along the atopic march (atopic dermatitis, food allergy, asthma, allergic rhinitis). Conforming disorder nodes substitute the tissue-specific epithelium and lesion (e.g., filaggrin/keratinocyte in atopic dermatitis; bronchial epithelium and tight-junction loss in asthma; squamous esophageal epithelium in eosinophilic esophagitis). This is the cross-tissue counterpart of the gut-specific `intestinal_barrier_dysfunction` module. Key conformance target: `epithelial_barrier_dysfunction#Increased Transepithelial Allergen Penetration and Innate Immune Activation`.