Dataset Information

Antibiotics-Induced Dysbiosis of Intestinal Microbiota Aggravates Atopic Dermatitis in Mice by Altered Short-Chain Fatty Acids.

ABSTRACT:

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 × 10? CFU) or 100 ?L 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.

SUBMITTER: Kim HJ

PROVIDER: S-EPMC6875482 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Publications

Antibiotics-Induced Dysbiosis of Intestinal Microbiota Aggravates Atopic Dermatitis in Mice by Altered Short-Chain Fatty Acids.

Kim Ha Jung HJ Lee Seung Hwa SH Hong Soo Jong SJ

Allergy, asthma & immunology research 20200101 1

<h4>Purpose</h4>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.<h4>Methods</h4>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 (<i>Lactobacillus rhamnosus</i>, ...[more]

PMID: 31743970

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Project description:BackgroundEncephalitis, the inflammation of the brain, may be caused by an infection or an autoimmune reaction. However, few researches were focused on the gut microbiome characteristics in encephalitis patients.MethodsA prospective observational study was conducted in an academic hospital in Guangzhou from February 2017 to February 2018. Patients with encephalitis were recruited. Fecal and serum samples were collected at admission. Healthy volunteers were enrolled from a community. Disease severity scores were recorded by specialized physicians, including Glasgow Coma Scale (GCS), Sequential Organ Failure Assessment (SOFA), and Acute Physiology and Chronic Health Evaluation-II (APACHE-II). 16S rRNA sequence was performed to analyze the gut microbiome, then the α-diversities and β-diversities were estimated. Short-chain fatty acids (SCFAs) were extracted from fecal samples and determined by gas chromatography-mass spectrometry. Serum D-lactate (D-LA), intestinal fatty acid-binding protein (iFABP), lipopolysaccharide (LPS), and lipopolysaccharide-binding protein (LBP) were measured by enzyme-linked immunosorbent assay (ELISA). The associations among microbial indexes and clinical parameters were evaluated by Spearman correlation analysis.ResultsIn total, twenty-eight patients were recruited for analysis (median age 46 years; 82.1% male; median GCS 6.5; median SOFA 6.5; median APACHE-II 14.5). Twenty-eight age- and sex-matched healthy subjects were selected as controls. The β-diversities between patients and healthy subjects were significantly different. The α-diversities did not show significant differences between these two groups. In the patient group, the abundances of Bacteroidetes, Proteobacteria, and Bacilli were significantly enriched. Accordingly, fecal SCFA levels were decreased in the patient group, whereas serum D-LA, iFABP, LPS, and LBP levels were increased compared with those in healthy subjects. Correlation analyses showed that disease severity had positive correlations with Proteobacteria and Akkermansia but negative correlations with Firmicutes, Clostridia, and Ruminococcaceae abundances. The cerebrospinal fluid albumin-to-serum albumin ratio (CSAR) was positively related to the α-diversity but negatively correlated with the fecal butyrate concentration.ConclusionGut microbiota disruption was observed in encephalitis patients, which manifested as pathogen dominance and health-promoting commensal depletion. Disease severity and brain damage may have associations with the gut microbiota or its metabolites. The causal relationship should be further explored in future studies.

Dataset Information

Antibiotics-Induced Dysbiosis of Intestinal Microbiota Aggravates Atopic Dermatitis in Mice by Altered Short-Chain Fatty Acids.

Purpose

Methods

Results

Conclusions

Publications

Antibiotics-Induced Dysbiosis of Intestinal Microbiota Aggravates Atopic Dermatitis in Mice by Altered Short-Chain Fatty Acids.

Similar Datasets

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