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The medical word to watch in 2018: Dysbiosis

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By Warren R. Heymann, MD
Jan. 4, 2018

With increasing rapidity, new words enter the dermatological lexicon, reflecting concepts that change our perceptions of disease and treatment. Recent examples include “comorbidities,” “programmed cell death inhibition,” and “teledermatology”. The word to watch in 2018 is “dysbiosis.”

The microbiome has been the focus of intense research in dermatology. The term microbiota describes the microbial community of a given anatomic or environmental niche; microbiome may be used as a synonym for microbiota and for its genetic blueprint. Dermatologists are familiar with the prefix “dys”, meaning abnormal or impaired (e.g. “dysplasia” in atypical nevi, “dysesthesia” for a painful, burning sensation, or “dyspepsia” for the agita experienced when thinking about MACRA and MIPS). Dysbiosis refers to alterations in the microbiota associated with disease. (1)

The microbiome has been studied most extensively in atopic dermatitis (AD). The pathogenesis of AD is complex; Brunner et al have brilliantly reviewed the interplay between immunologic, microbial, and epithelial factors that lead to the phenotypic heterogeneity of AD. Their “key messages” are: 1) AD is centered on T-helper cell type 2, with variable activation of other immune axes depending on the population; 2) Filaggrin loss-of-function mutation is the strongest risk factor for AD, but is present in only a minority of patients (and rarely in African-Americans); 3) AD flares are associated with a decreased diversity of the skin microbiota together with an increased abundance of Staphylococcus aureus; 4) Skin commensal bacteria are protective against S. aureus through production of antimicrobial peptides — in AD there is a relative deficiency of these peptides, most likely due to down-regulation by IL-4 and IL-13; 5) Increases in blood inflammatory and cardiovascular mediators, abnormalities in nonlesional skin, and associated allergic and nonallergic comorbidities suggest the systemic nature of AD. (2)

Although dysbiosis appears to be a hallmark of AD, the composition of the skin microbiome and the causality of dysbiosis in eczema have not been precisely defined. In their systematic review, Bjerre et al found that the skin in AD had low bacterial diversity (lowest at dermatitis-involved sites). Three studies demonstrated depletion of Malassezia spp. and high non-Malassezia fungal diversity. The relative abundance of Staphylococcus aureus and Staphylococcus epidermidis were elevated and other genera were reduced, including Propionibacterium. A mouse study indicated that dysbiosis is a driving factor in eczema pathogenesis. The data are not sufficiently robust for good characterization; however, dysbiosis in AD not only implicates Staphylococcus spp., but also microbes such as Propionibacterium and Malassezia. The authors suggested that a causal role of dysbiosis in eczema in mice should encourage human studies to determine its relevance. (3)

Does AD lend itself to S aureus colonization or do the bacteria cause AD in predisposed patients? Meylan et al performed a prospective birth cohort study, characterizing the association between skin colonization and AD development in 149 white infants with or without a family history of atopy. They assessed infants clinically and collected axillary and antecubital fossa skin swabs for culture-based analysis at birth and at seven time points over the first 2 years of life. They found that at age 3 months, S. aureus was more prevalent on the skin of infants who subsequently developed AD. S. aureus prevalence was increased on infants’ skin at the time of AD onset and 2 months before it, when compared with age-matched, unaffected infants. Furthermore, at AD onset, infants testing positive for S. aureus were younger than uncolonized subjects. The authors concluded that specific changes in early-life skin colonization may actively contribute to clinical AD onset in infancy. (4) In the editorial that accompanies the article by Meylan et al, Williams and Gallo note that interactions among the skin microbiome (bacteria, fungi, and viruses), resident cells in the skin (keratinocytes, fibroblasts, adipocytes, neural elements, and vasculature), and bone marrow-derived cells of the immune system (dendritic cells, lymphocytes, and granulocytes) are essential for homeostasis in healthy skin. In AD, molecular or cellular defects in these systems are associated with disease.AD may manifest from an individual or combination of defective functions. In some patients, S. aureus may be causative. (5)

Maintaining a healthy barrier by moisturizing the skin, appropriate use of bleach baths, and treating secondary infection are cornerstones of managing AD, in addition to topical agents (steroids, calcineurin inhibitors, crisaborole) and systemic medications (steroids, cyclosporine, mycophenolate mofetil, and dupilumab). A further understanding of dysbiosis should diminish distress.

1. Sohn K, Underwood MA. Prenatal and postnatal administration of prebiotics and probiotics. Semin Fetal Neonatol Med 2017; 22: 284-9
2. Brunner Y, et al. Immunologic, microbial, and epithelial interactions in atopic dermatitis. Ann Allergy Asthma Immunol 2017; Nov 7 [Epub ahead of print]
3. Bjerre RD, et al. The role of the skin microbiome in atopic dermatitis: A systematic review. Br J Dermatol 2017; 177; 1272-8.
4. Meylan P, et al. Skin colonization by Staphylococcus aureus precedes the clinical diagnosis of AD in infancy. J Invest Dermatol 2017; 137: 2497-504.
5. Williams MR, Gallo RL. Evidence that human skin microbiome dysbiosis promotes atopic dermatitis. J Invest Dermatol 2017; 137: 2460-1.

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