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

Tjaša Hertiš Petek, Maya Petek, Tadej Petek, Nataša Marčun Varda, Tjaša Hertiš Petek, Maya Petek, Tadej Petek, Nataša Marčun Varda

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.

Keywords: diaper dermatitis; immunology; inflammation; microbiome; nappy rash; pH; pediatrics; probiotics; skin.

Conflict of interest statement

The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
A model of contact irritant diaper dermatitis. The first step involves the penetration of irritants through the skin which stimulates keratinocytes (KC) to release proinflammatory mediators interleukin 1 alpha (IL-1α) and tumor necrosis factor alpha (TNF-α). The entry of irritants and microorganisms is facilitated by damage of stratum corneum (SC) integrity by fecal enzyme degradation, overhydration and disruption of the lipid bilayer structure. The initial release of IL-1α and TNF-α promotes further production of cytokines and chemokines IL-1β, granulocyte macrophage-colony stimulating factor (GM-CSF), IL-6, IL-8, vascular endothelial growth factor (VEGF), migration of Langerhans cells (LC) to the dermis, production of collagenases (col.) and prostaglandin E (PGE) by fibroblasts (FB), vasodilatation of the blood vessels, upregulation of adhesion molecules on endothelial cells and the transmigration of inflammatory cells (TL—T lymphocyte, EOS—eosinophil, NEU—neutrophil, MAC—macrophage) to the epidermis. The net effect is inflammation and erythema of the skin. Probiotics present a protective shield against irritants, maintain a lower pH, secrete beneficial metabolites and block pathogen invasion.

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