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Evidence-Based Supplement Research
Evidence-Based Supplement Research

Study Design

Type
Randomized Controlled Trial (RCT)
Sample size
n = 9
Population
DNFB-induced AD mice
Methods
Controlled experimental study
  • Rigorous Journal
  • Animal Study

Abstract

Purpose: Emerging studies have reported gut microbial composition plays a key role in alleviating AD clinical symptoms during the probiotic intervention, but the correlation among clinical symptoms, immune responses and gut microbial alteration needs to be explored. Therefore, the objective was to investigate the correlation during Bifidobacterium adolescentis intervention in DNFB-induced AD mice.

Methods: The mice were randomly divided into nine groups and fed B. adolescentis for 3 weeks. At the end of the experiment, clinical and immune indicators were assessed. Flow cytometry was performed to explore the effect of B. adolescentis on regulatory T cells in the spleen. V3-V4 region of the 16S ribosomal RNA (rRNA) gene was sequenced to evaluate changes in the gut microbiota.

Results: Bifidobacteria adolescentis treatments reduced ear and skin thickness and suppressed eosinophils and mast cells infiltration. Th1- and Th2-type responses were regulated and the Tregs population was promoted in the spleen by B. adolescentis treatments. Bifidobacteria adolescentis increased the relative abundance of Lactobacillus but decrease Dorea and Pediococcus. Propionic and butyric acids were increased but isovaleric acid was decreased by B. adolescentis treatment. Besides, the functional modules, such as fatty acid biosynthesis, antigen processing and presentation were upregulated by B. adolescentis Ad1 treatment compared to the DNFB group.

Conclusion: Collectively, these results imply that B. adolescentis with the role of immunomodulation promotes Treg differentiation and suppresses Th2 responses, and increases the proportion of Lactobacillus that is positively correlated to increase in propionic acid production, and thus has the potential for AD amelioration.

Keywords: Atopic dermatitis; Bifidobacterium adolescentis; Gut microbiota; Immune responses; Short-chain fatty acids.

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