Abstract
The pathogenesis of atopic dermatitis (AD) involves complex factors, including gut microbiota and immune modulation, which remain poorly understood. The aim of this study was to restore gut microbiota via fecal microbiota transplantation (FMT) to ameliorate AD in mice. FMT was performed using stool from donor mice. The gut microbiota was characterized via 16S rRNA sequencing and analyzed using Quantitative Insights into Microbial Ecology 2 with the DADA2 plugin. Gut metabolite levels were determined by measuring fecal short-chain fatty acid (SCFA) contents. AD-induced allergic responses were evaluated by analyzing blood parameters (IgE levels and eosinophil percentage, eosinophil count, basophil percentage, and monocyte percentage), the levels of Th1 and Th2 cytokines, dermatitis score, and the number of mast cells in the ileum and skin tissues. Calprotectin level was measured to assess gut inflammation after FMT. FMT resulted in the restoration of gut microbiota to the donor state and increases in the levels of SCFAs as gut metabolites. In addition, FMT restored the Th1/Th2 balance, modulated Tregs through gut microbiota, and reduced IgE levels and the numbers of mast cells, eosinophils, and basophils. FMT is associated with restoration of gut microbiota and immunologic balance (Th1/Th2) along with suppression of AD-induced allergic responses and is thus a potential new therapy for AD.
Highlights
Atopic dermatitis (AD) is a chronic inflammatory skin disease known to affect ~15–30% of children and 10% of adults[1]
These results demonstrate that oral administration of 100 mg/ml streptomycin for 24 h most effectively depletes gut microbiota before fecal microbiota transplantation (FMT)
Infiltrated mast cells in the dorsal skin and ileum lesions were quantified by toluidine blue (TB) staining, and the results showed that the number of mast cells decreased in the FMT_8w group (p < 0.0001 and 0.0018, respectively; Fig. 7b, c)
Summary
Atopic dermatitis (AD) is a chronic inflammatory skin disease known to affect ~15–30% of children and 10% of adults[1]. The pathogenesis of AD is a complex combination of the immune response, impaired barrier function, and microbial factors, but it remains poorly understood[2]. Many studies have attributed changes in skin microbiota to immune modulation due to disturbances in epidermal barrier function[3]. There has been a recent focus on gut microbiota in association with immune modulation as a factor of interest in AD4. The gut microbiota is composed of 100 trillion resident bacteria and plays an important role in gut homeostasis and immunity[5]. Previous studies on AD have reported the effects of probiotic treatment on patients with AD through gut microbiota diversity manipulation or reduction, which were not always beneficial[3,11,12,13]
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