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dc.contributor.authorFajstová, Alena
dc.contributor.authorGalanova, Natalie
dc.contributor.authorCoufal, Stepan
dc.contributor.authorMalkova, Jana
dc.contributor.authorKostovcik, Martin
dc.contributor.authorCermakova, Martina
dc.contributor.authorPelantova, Helena
dc.contributor.authorKuzma, Marek
dc.contributor.authorŠedivá, Blanka
dc.contributor.authorHudcovic, Tomas
dc.contributor.authorHrncir, Tomas
dc.contributor.authorTlaskalova-Hogenova, Helena
dc.contributor.authorKverka, Miloslav
dc.contributor.authorKostovcikova, Klara
dc.date.accessioned2021-06-14T14:21:58Z-
dc.date.available2021-06-14T14:21:58Z-
dc.date.issued2020
dc.identifier.citationFAJSTOVÁ, 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.cs
dc.identifier.issn2073-4409
dc.identifier.uri2-s2.0-85098745079
dc.identifier.urihttp://hdl.handle.net/11025/43663
dc.format24 s.cs
dc.format.mimetypeapplication/pdf
dc.language.isoenen
dc.publisherMDPIen
dc.relation.ispartofseriesCellsen
dc.rights© MDPIen
dc.titleDiet Rich in Simple Sugars Promotes Pro-Inflammatory Response via GutMicrobiota Alteration and TLR4 Signalingen
dc.typečlánekcs
dc.typearticleen
dc.rights.accessopenAccessen
dc.type.versionpublishedVersionen
dc.description.abstract-translatedDiet 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.en
dc.subject.translatedinflammatory bowel diseasesen
dc.subject.translatedneutrophilsen
dc.subject.translatedmetabolitesen
dc.subject.translatedmicrobiomeen
dc.subject.translatedmucosal barrieren
dc.subject.translatedhigh-sugar dieten
dc.identifier.doi10.3390/cells9122701
dc.type.statusPeer-revieweden
dc.identifier.document-number601725700001
dc.identifier.obd43932919
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