Marrs, T. Pediatric Infectious Disease Journal. 35(11) pp. 1258–1261
Eczema (syn. “atopic eczema” or “atopic dermatitis”) affects at least one-fifth of the pediatric population in industrialized nations, often arises in early infancy and raises the risk of developing subsequent sensitization, food allergy and asthma. Pedigree studies of families carrying filaggrin loss-of-function mutations demonstrate a semi-dominant inheritance pattern for eczema. Filaggrin loss-of-function variants impair keratinocyte differentiation and reduce the ability of the skin to retain water, leading to poor skin barrier function and dry skin. However, it is not known what instigates the cutaneous inflammation associated with eczema, although bacterial pathogens and changes in the diversity of the cutaneous microbiota may play a role. Staphylococcus aureus is, for instance, commonly found on the skin of eczema sufferers, especially with more severe disease. However, it remains uncertain whether bacterial dysbiosis (microbial imbalance associated with reduced diversity and prominence of pathogenic strains) on the skin plays a causal role in the development of eczema and disease flares, or whether the observed expansion of S. aureus and reduction in bacterial diversity are primarily an epiphenomenon resulting from an impaired and inflamed skin barrier.
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