Publications by authors named "Hrncirova Lucia"

Article Synopsis
  • - The study focuses on metabolic dysfunction-associated steatotic liver disease (MASLD), which is linked to high fructose consumption and food preservatives like sodium benzoate, sodium nitrite, and potassium sorbate.
  • - Using a mouse model, researchers found that fructose combined with potassium sorbate worsened liver conditions, leading to increased fat, inflammation, and fibrosis in the liver, along with changes in gut microbiota and intestinal health.
  • - The results indicate that the interaction between diet, gut bacteria, and liver metabolism is complex, pointing to dietary changes and microbiome adjustments as potential strategies for preventing and treating MASLD.
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Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease. Its worldwide prevalence is rapidly increasing and is currently estimated at 24%. NAFLD is highly associated with many features of the metabolic syndrome, including obesity, insulin resistance, hyperlipidaemia, and hypertension.

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The worldwide incidence of many immune-mediated and metabolic diseases, initially affecting only the wealthy Western countries, is increasing rapidly. Many of these diseases are associated with the compositional and functional alterations of gut microbiota, i.e.

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The aim of this work was to test the hypothesis that antimicrobial food additives may alter the composition of human gut microbiota by selectively suppressing the growth of susceptible gut microbes. To explore the influence of antimicrobial food additives on the composition of the human gut microbiota, we examined the susceptibility of both aerobic and anaerobic gut bacteria to sodium benzoate, sodium nitrite, and potassium sorbate, and their combinations, using a broth microdilution method. The tested bacteria exhibited a wide range of susceptibilities to food additives.

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The world-wide incidence of many immune-mediated and metabolic diseases, including those of the intestines and liver, is steadily increasing. Gut microbiota plays a central role in the pathogenesis of these diseases as it mediates environmental changes to the intestinal immune system. Various environmental factors including diet, food additives and medication also trigger the compositional and functional alterations of microbiota, that is, dysbiosis, and this dysbiosis is closely associated with many chronic inflammatory diseases.

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Crohn's disease is a chronic immune-mediated intestinal inflammation targeted against a yet incompletely defined subset of commensal gut microbiota and occurs on the background of a genetic predisposition under the influence of environmental factors. Genome-wide association studies have identified about 70 genetic risk loci associated with Crohn's disease. The greatest risk for Crohn's disease represent polymorphisms affecting the CARD15 gene encoding nucleotide-binding oligomerization domain 2 (NOD2) which is an intracellular sensor for muramyl dipeptide, a peptidoglycan constituent of bacterial cell wall.

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Crohn's disease (CD) is an immune-mediated chronic intestinal disorder thought to be the result of an aggressive immune response to a subset of enteric bacteria in a genetically predisposed host. Numerous environmental factors are apparently involved in disease pathogenesis. Impaired ability of CD patients to control the gut microflora is associated with defects in the production of some antibacterial compounds (cryptdins) by epithelial cells.

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Autophagy is an integral part of cell strategy to overcome adverse living conditions. Moreover, autophagy participates in the protection of cytoplasm against invasion of the intracellular pathogenic bacteria. Abnormalities in the autophagy are participating on the inability of Crohn's disease patients to maintain gut microbiome homeostasis ultimating in the development of immunopathological reaction in these patients.

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