On the surface

Abstract

The commensal-epidermal homeostasis within healthy skin protects against allergic disease by inducing epidermal accumulation of commensal-specific type 1 and type 17 immune cells and increasing the expression of antimicrobial peptides and alarmins that target proallergic bacteria. The composition of skin microbiome and epidermal barrier integrity are interdependent, and disruption in one (eg, filaggrin mutations or dysbiosis) disrupts the other. Skin microbiome dysbiosis contributes to progression and exacerbation of allergic diseases, such as atopic dermatitis, food allergy, allergic rhinitis, and asthma. Current and potential treatments affecting the skin microbiome include emollients, restoration of skin commensals and antimicrobial peptides, and anti-T H 2 biologic therapy. Maintenance of the skin barrier is the primary prevention for the development or exacerbation of atopic disorders; however, studying preventions targeting the skin microbiome is needed.

Interferon-Lambda 1 Inhibits Staphylococcus aureus Colonization in Human Primary Keratinocytes

“…It is known that Th2-type cytokines (IL-4, IL-5, and IL-13) and epithelial-derived innate type-2 cytokines (TSLP) increased in skin lesions of acute stage of AD (DeVore et al, 2020;Edslev et al, 2020;Langan et al, 2020). TSLP is crucial for regulating the downstream IL-4/IL-13 and Th2 differentiation.…”

Strategies to Develop a Suitable Formulation for Inflammatory Skin Disease Treatment

“…For example, the Corynebacterium and Staphylococcus species predominate in moist microenvironments, while the Propionibacterium species is most present in the sebaceous glands. Allergic or inflammatory status may arise when changes in steady microbiome occur [ 47 , 48 , 49 ].…”

“…The term “commensal-epidermal homeostasis” means the homeostatic interactions between normal skin commensal microbiota and the epidermis physical barrier. The epidermis physical barrier prevents the invasion of external pathogens and provides habitation to the commensals [ 48 , 50 ]. For example, the natural moisturizing factors and metabolites from skin commensal microbiota contribute to acidic skin pH.…”

“…For example, the natural moisturizing factors and metabolites from skin commensal microbiota contribute to acidic skin pH. Therefore, failure to maintain acidic skin pH may alert the diversity of skin microbiota [ 48 ]. Therefore, the unbalance of commensal-epidermal homeostasis may affect the cross-talk of epidermal commensal-specific Th1 and Th17 cells and the secretion of antimicrobial peptides from keratinocytes and then lead to the barrier disruption [ 48 , 49 ].…”

“…Decreased commensals abundance may contribute to the progression and exacerbation of inflammatory skin diseases, such as atopic dermatitis [ 48 ]. However, studies reported that the richness and diversity of skin microbiota could be reversed by topical emollients [ 51 , 52 , 53 , 54 ].…”