An Inflammatory-Driven Ex Vivo Human Skin Model to Mimic Atopic Dermatitis–Like Barrier Dysfunction.
Author: Ana Lucia Pinheiro, Barbara Carli, Gabriela da Silva Leite, Gustavo Henrique da Silva, Thatiane Yoshie Kanazawa, Andrea Colombo Missiato, Giovana Valim Albigesi, Kelen Fabiola Arroteia, Samara Eberlin, Carla Monserrat Grecco Lopes
Published at: January 01, 1900
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease involving epidermal barrier dysfunction, immune dysregulation, and altered host–microbiome interactions. Central to its pathogenesis is a Th2-skewed immune response, characterized by elevated levels of interleukin-4 (IL-4) and interleukin-13 (IL-13), which directly impair keratinocyte differentiation and downregulate epidermal key structural proteins such as filaggrin. The resulting barrier disruption promotes increased transepidermal water loss, enhanced penetration of allergens and irritants, and heightened susceptibility to microbial colonization, perpetuating a vicious cycle of inflammation and barrier impairment.