Immunologic, microbial, and epithelial interactions in atopic dermatitis

Abstract

Recent clinical investigation has significantly expanded our knowledge on disease pathogenesis in atopic dermatitis, and current and future clinical trials will most likely further help to elucidate this complex, heterogeneous skin disease.

Moisturizers versus Current and Next-Generation Barrier Repair Therapy for the Management of Atopic Dermatitis

“…Another consequence of the flawed barrier in AD further linking the barrier defect to the characteristic immunophenotype in AD, is the so-called “cytokine cascade” [14]. In response to the sustained barrier defect, the epidermis produces a series of signaling molecules, including a host of cytokines and growth factors, in an inherently unsuccessful attempt to restore normal function [15].…”

Efficacy and safety of mepolizumab administered subcutaneously for moderate to severe atopic dermatitis

“…1,2 Neutralization of IL-5 is thought to reduce the production and survival of eosinophils which may be therapeutic in subjects with atopic dermatitis (AD). [3][4][5] We conducted a multicenter, randomized, double-blind, placebo-controlled, parallel-group Phase-2 clinical trial to investigate the efficacy and safety of 100 mg mepolizumab administered subcutaneously (SC). The study consisted of a prescreening period (≤4 weeks), a screening period (≤2 weeks), a 16-week treatment period, and a follow-up period (≤4 weeks).…”

The role of phosphodiesterase 4 in the pathophysiology of atopic dermatitis and the perspective for its inhibition

“…In addition to changes in immune cells, AD is associated with skin barrier dysfunction characterized by increased stratum corneum pH, increased transepidermal water loss and decreased stratum corneum hydration . Epidermal abnormalities include defects in terminal differentiation of keratinocytes, as well as epidermal hyperplasia and induction of S100As . In addition to dysfunction in the synthesis of ceramides, reduced skin hydration in AD has also been associated with decreased sebum production suggesting that this contributes to skin barrier dysfunction …”

“…[61] Epidermal abnormalities include defects in terminal differentiation of keratinocytes, as well as epidermal hyperplasia and induction of S100As. [33,62,63] In addition to dysfunction in the synthesis of ceramides, reduced skin hydration in AD has also been associated with decreased sebum production suggesting that this contributes to skin barrier dysfunction. [61] The skin microbiome can also play a role in the pathophysiology of AD.…”