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Randomized Controlled Trial
. 2018 Feb 28;13(2):e0192443.
doi: 10.1371/journal.pone.0192443. eCollection 2018.

Emollient use alters skin barrier and microbes in infants at risk for developing atopic dermatitis

Affiliations
Randomized Controlled Trial

Emollient use alters skin barrier and microbes in infants at risk for developing atopic dermatitis

Martin Glatz et al. PLoS One. .

Abstract

Background: Emollients are a mainstay of treatment in atopic dermatitis (AD), a disease distinguished by skin bacterial dysbiosis. However, changes in skin microbiota when emollients are used as a potential AD preventative measure in infants remain incompletely characterized.

Results: We compared skin barrier parameters, AD development, and bacterial 16S ribosomal RNA gene sequences of cheek, dorsal and volar forearm samples from 6-month-old infants with a family history of atopy randomized to receive emollients (n = 11) or no emollients (controls, n = 12). The emollient group had a lower skin pH than the control group. The number of bacterial taxa in the emollient group was higher than in the control group at all sites. The Streptococcus salivarius proportion was higher in the emollient versus control groups at all sites. S. salivarius proportion appeared higher in infants without AD compared to infants with AD. A decrease in S. salivarius abundance was further identified in a separate larger population of older children demonstrating an inverse correlation between AD severity at sampling sites and S. salivarius proportions.

Conclusions: The decreased skin pH and the increased proportion of S. salivarius after long-term emollient use in infants at risk for developing AD may contribute to the preventative effects of emollients in high-risk infants.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Skin assessments in infants who received emollients as compared to controls.
(A) Skin pH, (B) transepidermal water loss and (C) water capacitance shown as mean ± standard error of the mean. *P < 0.05 (Wilcoxon rank sum test).
Fig 2
Fig 2. Diversity indices of skin bacterial communities.
(A) Chao richness and (B) Shannon diversity shown as mean ± standard error of the mean. *P < 0.01 (Wilcoxon rank sum test). (C) The Yue-Clayton similarity index at the cheek, plotted in a principal coordinate analysis (PCoA). Samples from the right and the left body site are shown separately. Percentage variation attributed to PCoA axes are indicated at the axis labels. Biplot arrows indicate bacterial taxa significantly contributing to dissimilarity between samples, the lengths of arrows indicate the amount of contribution to dissimilarity along axis 1 (Spearman correlation). Letter codes for bacterial taxa, Spearman correlations with axes and associated P-values are shown in Table 1.
Fig 3
Fig 3. Bacterial taxonomic classifications in the skin of infants aged 6 months.
(A) Relative abundance of order-genera that represented >1% of total 16S rRNA sequences with additional species level resolution for the two most abundant Streptococcus spp. Each bar represents the relative abundance of bacteria averaged from the right and left sides of each infant. (B) Relative abundance of Streptococcus salivarius in both infant groups separated by sampling site. The data are shown as the mean ± standard error of the mean. *P < 0.05 (Wilcoxon rank sum test).
Fig 4
Fig 4. Relative abundance of Streptococcus salivarius in infants with atopic dermatitis (AD) versus without AD.
(A) Relative abundance of Streptococcus salivarius in infants that did not receive emollients (A) Relative abundance of S. salivarius in children with AD (n = 12) at three disease states: baseline, flare, postflare; and in healthy control children. Data in (A) and (B) are shown as mean ± standard error of the mean. All comparisons are not statistically significant (P>0.05).

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