Skin Barrier Function in Atopic Dermatitis
Recent approaches to explore the pathogenic etiologies of atopic dermatitis using molecular genetic techniques have revealed underlying abnormalities in skin barrier function. Primary cutaneous barrier function is maintained by several physiological factors, including proper skin permeability that is regulated by both the stratum corneum barrier and the tight junction barrier and innate immune response of secretion from both the skin and skin appendages. The corneocyte lipid envelope and natural moisturizing factors derived from filaggrin prevent skin dryness and function in pathogen control. Epidermal tight junctions are composed of claudin-1, which comprises a water barrier correlated with its expression level. Secretions, such as sebum and sweat, contribute to decrease the impact of environmental stimuli (e.g., antigens, detergents, proteases, heat, and mechanical stimuli) to maintain the moistness of the stratum corneum and to regulate temperature. Disruption or dysfunction of these mechanisms impairs skin homeostasis and allows the invasion of pathogens from outside. Development of internal inflammation causes external barrier disruption in turn. This vicious cycle contributes to the chronic inflammation of atopic dermatitis. Appropriate guidance with a main focus on barrier restoration will restrain recurrence of the symptoms. This chapter reviews the barrier function of skin in atopic dermatitis.
KeywordsAtopic dermatitis Barrier Filaggrin Tight junction Claudins Stratum corneum Anti-microbial peptides Corneocyte lipid envelope
Conflict of Interest
The authors have no conflicts of interest to declare.
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