Emerging Links between Microbiome Composition and Skin Immunology in Diaper Dermatitis: A Narrative Review

Abstract

Diaper dermatitis is a common type of irritant contact dermatitis occurring in infants and toddlers. Its occurrence is triggered by an unfavorable environment under the diaper, damage to skin integrity by fecal enzyme degradation, overhydration and disruption of the lipid bilayer structure facilitating the entry of irritants and microorganisms. In diaper dermatitis development, the central proinflammatory cytokines are IL-1α, IL-8 and TNF-α. The initial release of IL-1α and TNF-α starts a further cascade of pro-inflammatory chemo- and cytokines, resulting in inflammation and erythema of the skin. A recently recognized factor in diaper dermatitis is the composition of the skin microbiome; common pathogenic strains Candida albicans and Staphylococcus aureus are associated with skin irritation. The resulting impaired microbiome composition produces a local inflammatory response and may thus worsen the initial dermatitis clinical presentation and subsequent healing. Introduction of probiotics is an attractive treatment for microbiome modulation, which has shown success in other skin conditions in adults and children. Probiotics are thought to work as a protective shield against irritants, maintain low skin pH, secrete beneficial metabolites, and block pathogen invasion. There is preliminary evidence that certain probiotics given orally or topically could be used as a gentle intervention in diaper dermatitis.

The multi‐factorial modes of action of urease in the pathogenesis of incontinence associated dermatitis

“…It is believed that skin inflammation is triggered by chronic exposure to urinary/faecal irritants, causing epidermal keratinocytes to release pro-inflammatory cytokines. 4,21,22 The specific irritants are not currently known but this study is important in showing that ammonia itself is the likely cause. This suggests that early treatment of IAD should focus on the specific damage caused by ammonia itself, either by inhibiting its production and/or sequestrating it by forming a nonirritant adduct.…”

“…It has been suggested in the literature that chronic exposure to urinary/faecal irritants causes epidermal keratinocytes to release growth factors and pro‐inflammatory cytokines, including IL‐1α, IL‐8 and TNF‐α. 4 , 21 , 22 The process is complex, initially prolonged exposure of skin to urine and/or faeces creates a moist environment. With time, skin maceration can occur which involves hyperhydration of keratinocytes and disruption of intercellular lipid bilayers.…”

mirada a las dermatosis de pañal

“…BMC Dermatol. 2020;20(1):7. https://doi.org/10.1186/s12895-020-00104-z los queratinocitos la producción de mediadores proinflamatorios, especialmente interleucina 1α (IL-1α) y factor de necrosis tumoral α (FNT-α), los cuales, a su vez, aumentan la producción de citocinas y quimiocinas como la IL-1β, IL-6, IL-8, el factor estimulante de colonias de macrófagos y granulocitos (GM-CSF) y el factor de crecimiento endotelial vascular (VEGF), que generan migración de células de Langerhans y células inflamatorias, producción de colagenasas y prostaglandina E, lo que produce vasodilatación y aumento de las moléculas de adhesión endotelial (13,14) .…”

“…El microbioma cutáneo hace parte de la primera barrera de defensa (sistema inmunitario innato), ya que bloquea la invasión por microorganismos patógenos, secretando metabolitos beneficiosos que mantienen el pH bajo. Estudios recientes proponen el uso de probióticos como parte del manejo, aunque hasta la fecha no se cuenta con ensayos clínicos controlados y aleatorizados que respalden esta estrategia (12,13,16) . Además, la lactancia materna exclusiva ha demostrado prevenir la DP (17) debido a que las heces de estos niños tienen un pH más bajo y una baja actividad de las lipasas y proteasas, lo que las hace menos irritantes (18,19) .…”

Development and Microbiological Evaluation of Natural Diaper Rash (Diaper Dermatitis) Cream Formulations

“…However, the interaction of other factors facilitates the access of microorganisms to the epidermis through the damaged stratum corneum (SC) layer, which increases the risk of secondary infections caused by fungi and bacteria (5). When secondary infection develops, the course of gland dermatitis becomes more severe (6).…”