ALLERGENS (RK BUSH AND JA WOODFOLK, SECTION EDITORS) The Role of the Skin Microbiome in Atopic Dermatitis Michael R. Williams 1 & Richard L. Gallo 1 Published online: 24 September 2015 # Springer Science+Business Media New York 2015 Abstract Atopic dermatitis (AD) is a common skin disease that affects a large proportion of the population worldwide. The incidence of AD has increased over the last several de- cades along with AD’ s burden on the physical and psycholog- ical health of the patient and family. However, current ad- vances in understanding the mechanisms behind the patho- physiology of AD are leading to a hopeful outlook for the future. Staphylococcus aureus (S. aureus) colonization on AD skin has been directly correlated to disease severity but the functions of other members of the skin bacterial commu- nity may be equally important. Applying knowledge gained from understanding the role of the skin microbiome in main- taining normal skin immune function, and addressing the det- rimental consequences of microbial dysbiosis in driving in- flammation, is a promising direction for development of new treatments. This review discusses current preclinical and clin- ical research focused on determining how the skin microbiome may influence the development of AD. Keywords Skin microbiome . Dysbiosis . Atopic dermatitis . Staphylococcus aureus . Staphylococcus epidermidis . Virulence factors Introduction Atopic dermatitis (AD) is a chronic allergic skin disease the includes frequent flares, and manifests with characteristic findings of dry, red, and pruritic skin in a typical distribution [1]. AD is one of the most common skin disorders and affects 5–20 % of infants worldwide with lesser prevalence in adult- hood [2]. Although AD is rarely lethal, several studies have shown that AD frequently leads to a severely compromised way of life for patients and their families and thus is a major health care burden [3, 4]. Furthermore, AD often associates with other allergic diseases including asthma and allergic rhi- nitis [5], thus further compounding the importance of this disease. Finally, the number of infants and adults affected by AD is higher in industrialized nations and has also grown over the past several decades. Many suspect that a link to excessive hygiene in these industrialized regions leads to a lack of ben- eficial host immune education provided by microbes on or within the body [6, 7]. Understanding the mechanisms behind AD and ways to treat it are therefore extremely important and highly relevant topics in the fields of allergy and dermatology. Both genetic and environmental factors play a substantial role in the onset of AD. Genome-wide scans have revealed that there are several shared chromosome loci among AD patients where gene expression has been altered. These stud- ies, however, clearly demonstrate that AD is a complex dis- ease with many potential genetic factors at play [1]. Specific genetic mutations that have been linked to AD Include genes involved in formation of the epidermal skin barrier such as filaggrin (FLG), genes involved in tight junctions (TJs), and the serine protease inhibitor Kazal-type 5 (SPINK5) [8–12]. Mutations in T helper cell 2 (Th2) cytokines IL-4 and IL-13 have also been correlated in AD pathogenesis [13, 14]. In most cases, data support that environmental factors including food and aeroallergens, as well as physical stressors including This article is part of the Topical Collection on Allergens * Richard L. Gallo rgallo@ucsd.edu Michael R. Williams mrw006@ucsd.edu 1 Department of Dermatology, University of California San Diego, 9500 Gillman Dr., #0869, La Jolla, CA 92093, USA Curr Allergy Asthma Rep (2015) 15: 65 DOI 10.1007/s11882-015-0567-4