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Diet Rich in Simple Sugars Promotes Pro-Inflammatory Response via Gut Microbiota Alteration and TLR4 Signaling
A. Fajstova, N. Galanova, S. Coufal, J. Malkova, M. Kostovcik, M. Cermakova, H. Pelantova, M. Kuzma, B. Sediva, T. Hudcovic, T. Hrncir, H. Tlaskalova-Hogenova, M. Kverka, K. Kostovcikova
Language English Country Switzerland
Document type Journal Article, Research Support, Non-U.S. Gov't
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PubMed
33339337
DOI
10.3390/cells9122701
Knihovny.cz E-resources
- MeSH
- Chronic Disease MeSH
- Diet * MeSH
- DNA-Binding Proteins deficiency metabolism MeSH
- Feces MeSH
- Colitis genetics immunology pathology MeSH
- Monosaccharides adverse effects MeSH
- Mice, Inbred BALB C MeSH
- Permeability MeSH
- Gene Expression Regulation MeSH
- Signal Transduction * MeSH
- Dextran Sulfate MeSH
- Immunity, Mucosal MeSH
- Intestines pathology MeSH
- Gastrointestinal Microbiome * MeSH
- Severity of Illness Index MeSH
- T-Lymphocytes immunology MeSH
- Toll-Like Receptor 4 metabolism MeSH
- Inflammation microbiology pathology MeSH
- Animals MeSH
- Check Tag
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Diet is a strong modifier of microbiome and mucosal microenvironment in the gut. Recently, components of western-type diets have been associated with metabolic and immune diseases. Here, we studied how high-sugar diet (HSD) consumption influences gut mucosal barrier and immune response under steady state conditions and in a mouse model of acute colitis. We found that HSD significantly increased gut permeability, spleen weight, and neutrophil levels in spleens of healthy mice. Subsequent dextran sodium sulfate administration led to severe colitis. In colon, HSD significantly promoted neutrophil infiltration and increased the levels of IL-6, IL-1β, and TNF-α. Moreover, HSD-fed mice had significantly higher abundance of pathobionts, such as Escherichia coli and Candida, in fecal samples. Although germ-free mice colonized with microbiota of conventionally reared mice that consumed different diets had equally severe colitis, mice colonized with HSD microbiota showed markedly increased infiltration of neutrophils to the gut. The induction of colitis in Toll-like receptor 4 (TLR4)-deficient HSD-fed mice led to significantly milder colitis than in wild-type mice. In conclusion, our results suggested a significant role of HSD in disruption of barrier integrity and balanced mucosal and systemic immune response. In addition, these processes seemed to be highly influenced by resident potentially pathogenic microbiota or metabolites via the TLR4 signaling pathway.
References provided by Crossref.org
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- $a Diet is a strong modifier of microbiome and mucosal microenvironment in the gut. Recently, components of western-type diets have been associated with metabolic and immune diseases. Here, we studied how high-sugar diet (HSD) consumption influences gut mucosal barrier and immune response under steady state conditions and in a mouse model of acute colitis. We found that HSD significantly increased gut permeability, spleen weight, and neutrophil levels in spleens of healthy mice. Subsequent dextran sodium sulfate administration led to severe colitis. In colon, HSD significantly promoted neutrophil infiltration and increased the levels of IL-6, IL-1β, and TNF-α. Moreover, HSD-fed mice had significantly higher abundance of pathobionts, such as Escherichia coli and Candida, in fecal samples. Although germ-free mice colonized with microbiota of conventionally reared mice that consumed different diets had equally severe colitis, mice colonized with HSD microbiota showed markedly increased infiltration of neutrophils to the gut. The induction of colitis in Toll-like receptor 4 (TLR4)-deficient HSD-fed mice led to significantly milder colitis than in wild-type mice. In conclusion, our results suggested a significant role of HSD in disruption of barrier integrity and balanced mucosal and systemic immune response. In addition, these processes seemed to be highly influenced by resident potentially pathogenic microbiota or metabolites via the TLR4 signaling pathway.
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