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

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F49777513%3A23520%2F20%3A43961920" target="_blank" >RIV/49777513:23520/20:43961920 - isvavai.cz</a>

  • Alternative codes found

    RIV/61388971:_____/20:00537701 RIV/61989592:15310/20:73604995 RIV/00216208:11310/20:10422268

  • Result on the web

    <a href="https://www.mdpi.com/2073-4409/9/12/2701" target="_blank" >https://www.mdpi.com/2073-4409/9/12/2701</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/cells9122701" target="_blank" >10.3390/cells9122701</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

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

  • Original language description

    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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10601 - Cell biology

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2020

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Cells

  • ISSN

    2073-4409

  • e-ISSN

  • Volume of the periodical

    9

  • Issue of the periodical within the volume

    12

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    24

  • Pages from-to

  • UT code for WoS article

    000601725700001

  • EID of the result in the Scopus database

    2-s2.0-85098745079