Diet Rich in Simple Sugars Promotes Pro-Inflammatory Response via Gut Microbiota Alteration and TLR4 Signaling

0537701 - MBÚ 2021 RIV CH eng J - Journal Article
Fajstová, Alena - Galanová, Natálie - Coufal, Štěpán - Málková, Jana - Kostovčík, Martin - Čermáková, Martina - Pelantová, Helena - Kuzma, Marek - Šedivá, Blanka - Hudcovic, Tomáš - Hrnčíř, Tomáš - Tlaskalová-Hogenová, Helena - Kverka, Miloslav - Kostovčíková, Klára
Diet Rich in Simple Sugars Promotes Pro-Inflammatory Response via Gut Microbiota Alteration and TLR4 Signaling.
Cells. Roč. 9, č. 12 (2020), č. článku 2701. E-ISSN 2073-4409
R&D Projects: GA ČR(CZ) GJ17-06632Y; GA ČR(CZ) GA19-08294S; GA ČR(CZ) GA20-03997S; GA MZd(CZ) NV18-01-00040
Institutional support: RVO:61388971
Keywords : inflammatory bowel diseases * neutrophils * metabolites * microbiome * mucosal barrier * high-sugar diet
OECD category: Immunology
Impact factor: 6.600, year: 2020
Method of publishing: Open access
https://www.mdpi.com/2073-4409/9/12/2701

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.
Permanent Link: http://hdl.handle.net/11104/0315562