Title: Diet Rich in Simple Sugars Promotes Pro-Inflammatory Response via GutMicrobiota Alteration and TLR4 Signaling
Authors: Fajstová, Alena
Galanova, Natalie
Coufal, Stepan
Malkova, Jana
Kostovcik, Martin
Cermakova, Martina
Pelantova, Helena
Kuzma, Marek
Šedivá, Blanka
Hudcovic, Tomas
Hrncir, Tomas
Tlaskalova-Hogenova, Helena
Kverka, Miloslav
Kostovcikova, Klara
Citation: FAJSTOVÁ, A., GALANOVA, N., COUFAL, S., MALKOVA, J., KOSTOVCIK, M., CERMAKOVA, M., PELANTOVA, H., KUZMA, M., ŠEDIVÁ, B., HUDCOVIC, T., HRNCIR, T., TLASKALOVA-HOGENOVA, H., KVERKA, M., KOSTOVCIKOVA, K. Diet Rich in Simple Sugars Promotes Pro-Inflammatory Response via GutMicrobiota Alteration and TLR4 Signaling. Cells, 2020, roč. 9, č. 12. ISSN 2073-4409.
Issue Date: 2020
Publisher: MDPI
Document type: článek
article
URI: 2-s2.0-85098745079
http://hdl.handle.net/11025/43663
ISSN: 2073-4409
Keywords in different language: inflammatory bowel diseases;neutrophils;metabolites;microbiome;mucosal barrier;high-sugar diet
Abstract in different language: 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-1 beta, and TNF-alpha. 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.
Rights: © MDPI
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