The Role of the Environment and Exposome in Atopic Dermatitis

Abstract

Purpose of review Atopic dermatitis (AD) is a chronic inflammatory skin disorder affecting up to 20% of children and up to 5% of adults worldwide, contributing to significant disease-related morbidity in this patient cohort. Its aetiopathogenesis is underpinned by multiple factors, including genetic susceptibility, skin barrier defects, a skewed cutaneous immune response and microbiome perturbation in both the skin and the gut. In this review, we aim to examine the biological effects of key environmental exposures (the sum of which is termed the “exposome”) at the population, community and individual levels in order to describe their effect on AD pathogenesis. Recent findings It is now understood that as well as considering the type of environmental exposure with regard to its effect on AD pathogenesis, the dosage and timing of the exposure are both critical domains that may lead to either exacerbation or amelioration of disease. In this review, we consider the effects of population-wide exposures such as climate change, migration and urbanization; community-specific exposures such as air pollution, water hardness and allergic sensitisation; and individual factors such as diet, microbiome alteration, psychosocial stress and the impact of topical and systemic therapy. Summary This review summarises the interaction of the above environmental factors with the other domains of AD pathogenesis, namely, the inherent genetic defects, the skin barrier, the immune system and the cutaneous and gut microbiota. We specifically emphasise the timing and dosage of exposures and its effect on the cellular and molecular pathways implicated in AD.

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“…Atopic dermatitis (AD), the most common form of eczema, is a chronic inflammatory skin disease characterized by symptoms such as pruritic lesions, pain, and sleep disturbances [1,15]. AD onset points towards a complex interaction between skin barrier dysfunction, immune dysregulation, environmental risk factors, and dysbiosis of the intestinal and skin microbiota, which correlates with the clinical severity of AD [1,14,15,61].…”

“…Atopic dermatitis (AD), the most common form of eczema, is a chronic inflammatory skin disease characterized by symptoms such as pruritic lesions, pain, and sleep disturbances [1,15]. AD onset points towards a complex interaction between skin barrier dysfunction, immune dysregulation, environmental risk factors, and dysbiosis of the intestinal and skin microbiota, which correlates with the clinical severity of AD [1,14,15,61]. Through the gut-skin axis, intestinal dysbiosis has been shown to negatively impact skin function either through an increase of epithelial permeability, via pro-inflammatory cytokines, thus promoting immune dysregulation and contributing to the chronic systemic inflammation in AD, as by perpetuating pruritus via secretion of neuroendocrine itch mediators, leading to a chronic itch-scratch cycle, thus further disrupting the skin barrier [1,5,6,9].…”

“…Diet has a fundamental role in the homeostasis of bodily functions, including the functions of the skin, which, as an essential protective barrier, plays a crucial role in this balance [1][2][3]. The skin and intestine appear to share a series of indirect metabolic pathways in a dual relationship known as the "gut-skin axis" [4][5][6].…”

“…AD has been associated with an exacerbated skin response to environmental agents, characterized by relevant symptoms including pruritic lesions with typical morphology, pain, and sleep disturbances [1,14]. The onset of AD points towards a complex interaction between skin barrier dysfunction, immune dysregulation, environmental risk factors, and (intestinal and skin) dysbiosis [1,5,6,15].…”

“…AD has been associated with an exacerbated skin response to environmental agents, characterized by relevant symptoms including pruritic lesions with typical morphology, pain, and sleep disturbances [1,14]. The onset of AD points towards a complex interaction between skin barrier dysfunction, immune dysregulation, environmental risk factors, and (intestinal and skin) dysbiosis [1,5,6,15]. Intestinal dysbiosis seems to increase epithelial permeability via pro-inflammatory cytokines, promote immune dysregulation, and intensify the chronic systemic inflammation in AD [4][5][6][7]9,16].…”