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Published on: May 2, 2018
Antibiotics-Induced Dysbiosis of Intestinal Microbiota Aggravates Atopic Dermatitis in Mice by Altered Short-Chain
Ha Jung Kim1, Seung Hwa Lee2, Soo Jong Hong3,4
1Department of Internal Medicine, College of Veterinary Medicine, Chonnam National University, Gwangju, Korea.
Purpose:
Alterations in the intestinal microbiota in early life affects the development of atopic dermatitis (AD) in humans. This study aimed to further investigate the effects of gut dysbiosis in early life in an ovalbumin (OVA)-induced mouse model of AD.
Methods:
The AD mouse model was developed by serial OVA sensitization and mice were treated with an antibiotic cocktail in their drinking water for 2 weeks before primary sensitization. Probiotics (Lactobacillus rhamnosus, 1 × 10⁹ CFU) or 100 μL of fresh fecal supernatant were orally administered daily from 1 week before the first sensitization until the end of the study.
Results:
The AD mice which received antibiotics had significantly aggravated phenotypes, including clinical score, transepidermal water loss, and histopathology, compared to those treated with healthy feces or probiotics. Total systemic immunoglobulin E production and skin interleukin (IL) 4 levels were significantly increased in the antibiotic-treated mice compared to the other groups. Antibiotic treatment also increased the levels of IL17 and group 3 innate lymphoid cells (ILC3) in the gut and significantly suppressed the production of short-chain fatty acids (SCFAs) and decreased the number FOXP3⁺ cells.
Conclusions:
Our results suggest that the status of the gut microbiota in early life in the mouse may play a crucial role in AD development through intestinal SCFA production through regulate the numbers of CD4⁺IL17⁺/CD4⁺FOXP3⁺ regulatory T cells and ILC3s.
Insights
Early life gut dysbiosis worsens atopic dermatitis (AD) in mice. Antibiotic treatment increased AD severity, indicating the gut microbiota
Area of Science:
- Microbiology
- Immunology
- Dermatology
Background:
- Early-life intestinal microbiota alterations are linked to atopic dermatitis (AD) development.
- Gut dysbiosis in early life may influence AD pathogenesis.
Purpose of the Study:
- Investigate the impact of early-life gut dysbiosis on an ovalbumin (OVA)-induced mouse model of AD.
- Determine the role of specific microbial interventions in modulating AD phenotypes.
Main Methods:
- Established an OVA-induced AD mouse model.
- Administered an antibiotic cocktail to induce gut dysbiosis.
- Treated mice with probiotics (Lactobacillus rhamnosus) or fecal supernatant.
- Assessed clinical scores, transepidermal water loss, histopathology, IgE levels, and cytokine profiles.
Main Results:
- Antibiotic-induced dysbiosis significantly aggravated AD phenotypes and increased systemic IgE and skin IL-4 levels.
- Antibiotic treatment elevated gut IL-17 and innate lymphoid cells (ILC3s), suppressed short-chain fatty acids (SCFAs), and reduced FOXP3+ cells.
- Probiotic or fecal supernatant treatments mitigated AD severity compared to antibiotic treatment.
Conclusions:
- Early-life gut microbiota status critically influences AD development in mice.
- Intestinal SCFA production by the gut microbiota regulates CD4+ T cell subsets (IL17+/FOXP3+) and ILC3s, impacting AD.
- Targeting the gut microbiota early in life may be a therapeutic strategy for AD.
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