The Role of the Microbiome and Microbiome-Derived Metabolites in Atopic Dermatitis and Non-Histaminergic Itch
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REVIEW ARTICLE
The Role of the Microbiome and Microbiome‑Derived Metabolites in Atopic Dermatitis and Non‑Histaminergic Itch Wei Li1 · Gil Yosipovitch2
© The Author(s) 2020
Abstract Recent advances in our understanding of the pathophysiology of atopic dermatitis (AD) have revealed that skin microbiome dysbiosis plays an important role in the disease. In this review, we describe how changes in the structure and function of the microbiome are involved in the pathogenesis of AD. We highlight recent data showing that differential changes in microbial diversity, both within and across communities from different body habitats (including the skin, gut, and oral mucosa), are associated with the development and severity of AD. We also describe recent evidence demonstrating that the metabolic activity of the skin microbiome can act as a regulator of inflammation, with alterations in the level of a skin microbiomederived tryptophan metabolite, indole-3-aldehyde (IAId), being shown to play a role in AD. The various mechanisms by which interactions between the microbiome and components of the non-histaminergic pathway result in itch in AD are also discussed.
1 Introduction Atopic dermatitis (AD) is a multifactorial pruritic inflammatory skin disease involving genetic, environmental, and immune factors. Since the 1970s, the incidence of AD has increased two- to threefold in industrialized countries [1]. The short time span over which this increase has been observed makes it unlikely that genetic factors have played a major role, and environmental factors appear to have been more important in driving this rise in cases. During recent years, great progress has been made toward increasing our understanding of the pathogenesis of AD. Skin barrier malfunction is a prominent feature of AD, but skin microbiome dysbiosis plays an equally important role in the disease mechanism [2]. Skin dysbiosis in AD is characterized by increased abundance of Staphylococcus aureus * Wei Li [email protected] * Gil Yosipovitch [email protected] 1
Department of Dermatology, Huashan Hospital, Fudan University, Shanghai 200040, China
Miami Itch Center, Dr Phillip Frost Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami, Miami, FL, USA
2
[3]. In the presence of this dysbiosis and barrier dysfunction, external stimuli such as infection, allergens, and mechanical injury lead to activation of skin keratinocytes to produce interleukin (IL)-33, IL-25, and thymic stromal lymphopoietin (TSLP), inducing differentiation of T helper type 2 (Th2) cells that secrete IL-4, IL-5, and IL-13 and resulting in Th2 inflammation [4, 5]. This inflammation can in turn activate keratinocytes, forming a vicious cycle that maintains skin inflammation in AD (Fig. 1). Thus, the skin microbiome, keratinocytes, Langerhans cells, and Th2 inflammation make up the skin microenvironment in AD. However, one of the features of AD is that it always precedes the onset of other atopic manifestations, including food allergie
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