4.7 Review

Association between barrier impairment and skin microbiota in atopic dermatitis from a global perspective: Unmet needs and open questions

Journal

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 148, Issue 6, Pages 1387-1393

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2021.10.002

Keywords

Allergic; atopy; asthma; allergic rhinitis; atopic march; phenotype; transepidermal water loss; hydration; Staphylococcus; epigenetic; interleukin

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Atopic diathesis is a prevalent condition with a wide range of clinical manifestations and age of onset, characterized by a common inherited epidermal barrier dysfunction. Microbiome diversity and contact with nonpathogenic microbes play a key role in immune system maturation and may impact the development of the disease.
Atopic diathesis encompassing atopic dermatitis (AD), allergic rhinoconjunctivitis, food allergy, eosinophilic esophagitis, and asthma is a widely prevalent condition with a broad heterogeneity in clinical course, age of onset, and lifespan persistence. A primary event in AD is the commonly inherited epidermal barrier dysfunction. Together with the hostmicrobiome interactions, barrier defect and allergen exposure modulate both innate and adaptive immunity, thus triggering and maintaining the inflammatory response. Microbiome diversity, together with the host's contact with nonpathogenic microbes in childhood, is a prerequisite for functional maturation of the immune system, which is in part mediated by microbiome-induced epigenetic changes. Yet, whether microbiome alterations are the result or the reason for barrier impairment and inflammatory response of the host is unclear. Exposure to locally prevalent microbial species could contribute to further modification of the disease course. The objective of this review is to reveal the link between changes in the skin microbiota, barrier dysfunction, and inflammation in AD. Addressing unmet needs includes determining the genetic background of AD susceptibility; the epigenetic modifications induced by the microbiota and other environmental factors; the role of globally diverse provoking factors; and the implementation of personalized, phenotype-specific therapies such as a epidermal barrier restoration in infancy and microbiota modulation via systemic or topical interventions, all of which open gaps for future research. (J Allergy Clin Immunol 2021;148:1387-93.)

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