Supplement Article: The Role of Epidermal Barrier Dysfunction and Cutaneous Microbiome Dysbiosis in the Pathogenesis and Management of Acne Vulgaris and Rosacea

September 2022 | Volume 21 | Issue 9 | SF3502915 | Copyright © September 2022


Published online August 31, 2022

Justin W. Marson MDa, Neal Bhatia MDb, Emmy Graber MD MBAc, Julie Harper MDd, Peter Lio MDe,f, Brook Tlougan MDg,h, Dillon Nussbaum BSi, Hilary E. Baldwin MDj,k

aDepartment of Dermatology, SUNY Downstate Health Sciences University, Brooklyn, NY;
bDirector of Clinical Dermatology, Therapeutics Clinical Research, San Diego, CA;
c The Dermatology Institute of Boston, Boston, MA;
dThe Dermatology and Skin Care Center of Birmingham, Birmingham AL;
eDepartments of Dermatology & Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL;
f Medical Dermatology Associates of Chicago, Chicago, IL;
g Westmed Medical Group, Purchase, NY;
hDepartment of Dermatology, Columbia University, New York, NY;
i Department of Dermatology, George Washington University, Washington, DC;
j Acne Treatment and Research Center, Brooklyn, NY;
k Department of Dermatology, Rutgers Robert Wood Johnson Medical Center, New Brunswick, NJ

Abstract
Background: Dysregulation of either the cutaneous microbiome (CM) or epidermal barrier function (EBF) is thought to play an increasingly important role in acne vulgaris (AV) and rosacea pathogenesis.
Objective: To review the literature regarding epidermal barrier dysfunction (EBD) and cutaneous dysbiosis in AV and rosacea and provide clinical pearls for dermatologists.
Methods: A Medline literature search was performed for relevant literature regarding EBD and dysbiosis and either AV or rosacea. An expert consensus panel was then convened to discuss article merits and distill findings into clinical pearls.
Results: Final review included 138 articles. Puberty may alter natural stratum corneum lipid ratios, instigating and/or exacerbating EBD in AV. Patients with severe AV have an abundance of virulent Cutibacterium acnes phylotype IA1. EBD may manifest as classic signs of rosacea and improve with treatment. While several microbial populations are dysregulated in rosacea, the effect from any singular species is unclear. Current AV and rosacea treatment regimens may mitigate inflammation but may also indiscriminately damage CM and EBF. Physiologic moisturizers and cleansers that harness pre-/pro-/postbiotics may have a role in restoring CM, EBF, and potentially improving dermatosis severity.
Limitations: Limited prospective clinical trial data especially regarding over-the-counter (OTC)/non-prescription skincare products. Conclusion: Appropriately developed prescription and OTC preparations may selectively influence the microbiome and potentially maintain/restore EBF. By understanding this relationship, dermatologists will be better able to educate patients on the importance of appropriate skin care.

J Drugs Dermatol. 2022;21:9(Suppl 2):s5-14.

INTRODUCTION

The cutaneous microbiome (CM) is a sprawling ecosystem comprising various microorganisms and their metabolites that dwell on every surface of the human body.1-4 Together, the human body and microbiome create a functional synergy that is increasingly thought to modulate local and systemic inflammation.

While CM composition varies with moisture, sebaceous gland activity, and anatomical region, these microbes exist symbiotically with other commensal organisms and the surfaces on which they dwell, receiving necessary nutrients (eg, amino acids, fatty acids, moisture) while providing a slightly acidic pH, priming host immune response (eg, induced antimicrobial peptides [AMP] and bacteriocins) and outcompeting classic pathogenic organisms (eg, pathogenic biofilm-producing, strains of Streptococcus epidermidis and Staphylococcus aureus).4-10 In this regard, the CM functions as a distinct, organized, and unique layer atop the stratum corneum (Figure 1).11

When appropriately functioning, the CM and the epidermal barrier exist in homeostasis.12-15 The loss of epidermal barrier function (EBF), dysbiosis, or both may result in a dysregulated inflammatory response, as is classically seen in atopic
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