Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1230401 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Riclin: A novel soluble dietary fiber for promoting gastric health and ameliorating gastric mucosal injury
| PRJNA1230083 | ENA
Project description:Focal and diffuse damage to the gastric mucosa contributes to gastric mucosal injury (GMI). Dietary fiber may exert protective effects against GMI; however, its use as a gastrointestinal intervention remains limited. Here, we assessed the potential role of dietary fiber Riclin in GMI. Dietary fiber Riclin exerted a dual effect in enhancing gastric mucosal defense. It modulated microbial-metabolite composition, enhancing biological barriers and reinforcing sustained adhesion to the gastric mucus bicarbonate barrier. Additionally, Riclin enhanced the gastric mucosal immune barrier through the NOD/TLR4/NF-κB pathway. The protective role of Riclin in GMI was revealed by constructing an alcohol-induced murine gastric ulcer model. Our results propose Riclin as a novel dietary fiber with the potential to ameliorate a wide range of gastric disorders characterized by a disrupted gastric mucosal defense and immune dysregulation. In particular, we underscore its potential as a promising dietary fiber for promoting gastric health.
2025-03-15 | GSE290768 | GEO
Project description:Despite accepted health benefits of dietary fiber, little is known about the mechanisms by which fiber deprivation impacts the gut microbiota and alters disease risk. Using a gnotobiotic model, in which mice were colonized with a synthetic human gut microbiota, we elucidated the functional interactions between dietary fiber, the gut microbiota and the colonic mucus barrier, which serves as a primary defence against pathogens. We show that during chronic or intermittent dietary fiber deficiency, the gut microbiota resorts to host-secreted mucus glycoproteins as a nutrient source, leading to erosion of the colonic mucus barrier. Dietary fiber deprivation promoted greater epithelial access and lethal colitis by the mucosal pathogen, Citrobacter rodentium, but only in the presence of a fiber-deprived microbiota that is pushed to degrade the mucus layer. Our work reveals intricate pathways linking diet, gut microbiome and intestinal barrier dysfunction, which could be exploited to improve health using dietary therapeutics. Germ-free mice (Swiss Webster) were colonized with synthetic human gut microbiota comprising of 14 species belonging to five different phyla (names of bacterial species: Bacteroides thetaiotaomicron, Bacteroides ovatus, Bacteroides caccae, Bacteroides uniformis, Barnesiella intestinihominis, Eubacterium rectale, Marvinbryantia formatexigens, Collinsella aerofaciens, Escherichia coli HS, Clostridium symbiosum, Desulfovibrio piger, Akkermansia muciniphila, Faecalibacterium prausnitzii and Roseburia intestinalis). These mice were fed either a fiber-rich diet or a fiber-free diet for about 6 weeks. The mice were then sacrificed and their cecal tissues were immediately flash frozen for RNA extraction. The extracted RNA was subjected to microarray analysis based on Mouse Gene ST 2.1 strips using the Affy Plus kit. Expression values for each gene were calculated using robust multi-array average (RMA) method.
2016-11-21 | GSE79067 | GEO
Project description:Omnivorous animals, including mice and humans, tend to prefer energy-dense nutrients rich in fat over plant-based diets, especially for short periods of time. The health consequences of this short-term consumption of energy-dense nutrients remain still unclear. We found that every short-term, reiterated switches to feast diets mimicking our social eating behavior, breached the potential buffering effect of the intestinal microbiota and deeply reorganized the immunological architecture of mucosa-associated lymphoid tissues. The first dietary switch was sufficient to induce transient mucosal immune depression and suppress systemic, antigen-specific immunity leading to higher susceptibility to Salmonella Typhimurium and Listeria monocytogenes infections. This was explained by a reduction of CD4+ T cell metabolic fitness and cytokine production due to impaired mTOR activity in response to withdrawal of microbial provision of fiber metabolites. Reintroducing dietary fiber efficiently rewired T cell metabolism and restored both mucosal and systemic CD4+ T cell functions and immunity. Finally, dietary intervention study in human volunteers confirmed the impact of short-term dietary switches on human CD4+ T cell functionality. This work reveals that short-term nutritional changes cause a drastic yet transient depression of both mucosal and systemic immunity, creating windows of opportunities for pathogenic infections.
2023-07-11 | GSE229088 | GEO
Project description:Omnivorous animals, including mice and humans, tend to prefer energy-dense nutrients rich in fat over plant-based diets, especially for short periods of time. The health consequences of this short-term consumption of energy-dense nutrients remain still unclear. We found that every short-term, reiterated switches to feast diets mimicking our social eating behavior, breached the potential buffering effect of the intestinal microbiota and deeply reorganized the immunological architecture of mucosa-associated lymphoid tissues. The first dietary switch was sufficient to induce transient mucosal immune depression and suppress systemic, antigen-specific immunity leading to higher susceptibility to Salmonella Typhimurium and Listeria monocytogenes infections. This was explained by a reduction of CD4+ T cell metabolic fitness and cytokine production due to impaired mTOR activity in response to withdrawal of microbial provision of fiber metabolites. Reintroducing dietary fiber efficiently rewired T cell metabolism and restored both mucosal and systemic CD4+ T cell functions and immunity. Finally, dietary intervention study in human volunteers confirmed the impact of short-term dietary switches on human CD4+ T cell functionality. This work reveals that short-term nutritional changes cause a drastic yet transient depression of both mucosal and systemic immunity, creating windows of opportunities for pathogenic infections.
2023-07-11 | GSE229087 | GEO
Project description:Omnivorous animals, including mice and humans, tend to prefer energy-dense nutrients rich in fat over plant-based diets, especially for short periods of time. The health consequences of this short-term consumption of energy-dense nutrients remain still unclear. We found that every short-term, reiterated switches to feast diets mimicking our social eating behavior, breached the potential buffering effect of the intestinal microbiota and deeply reorganized the immunological architecture of mucosa-associated lymphoid tissues. The first dietary switch was sufficient to induce transient mucosal immune depression and suppress systemic, antigen-specific immunity leading to higher susceptibility to Salmonella Typhimurium and Listeria monocytogenes infections. This was explained by a reduction of CD4+ T cell metabolic fitness and cytokine production due to impaired mTOR activity in response to withdrawal of microbial provision of fiber metabolites. Reintroducing dietary fiber efficiently rewired T cell metabolism and restored both mucosal and systemic CD4+ T cell functions and immunity. Finally, dietary intervention study in human volunteers confirmed the impact of short-term dietary switches on human CD4+ T cell functionality. This work reveals that short-term nutritional changes cause a drastic yet transient depression of both mucosal and systemic immunity, creating windows of opportunities for pathogenic infections.
2023-07-11 | GSE229086 | GEO
Project description:Omnivorous animals, including mice and humans, tend to prefer energy-dense nutrients rich in fat over plant-based diets, especially for short periods of time. The health consequences of this short-term consumption of energy-dense nutrients remain still unclear. We found that every short-term, reiterated switches to feast diets mimicking our social eating behavior, breached the potential buffering effect of the intestinal microbiota and deeply reorganized the immunological architecture of mucosa-associated lymphoid tissues. The first dietary switch was sufficient to induce transient mucosal immune depression and suppress systemic, antigen-specific immunity leading to higher susceptibility to Salmonella Typhimurium and Listeria monocytogenes infections. This was explained by a reduction of CD4+ T cell metabolic fitness and cytokine production due to impaired mTOR activity in response to withdrawal of microbial provision of fiber metabolites. Reintroducing dietary fiber efficiently rewired T cell metabolism and restored both mucosal and systemic CD4+ T cell functions and immunity. Finally, dietary intervention study in human volunteers confirmed the impact of short-term dietary switches on human CD4+ T cell functionality. This work reveals that short-term nutritional changes cause a drastic yet transient depression of both mucosal and systemic immunity, creating windows of opportunities for pathogenic infections.
2023-07-11 | GSE236786 | GEO
Project description:Purpose: Although dietary cellulose is considered health promoting, there is still a lack of understanding of cellular and molecular mechanisms. The aim of this study was to shed light on possible effects of the fiber on key players in intestinal homeostasis, including intestinal epithelial cells. Method: Mice were fed a diet containing cellulose as the only source of fiber (CD, control diet) or a fiber free diet (FFD, fiber-free diet) for four weeks and then treated with dextran sulphate sodium in the drinking water for five days. To ensure that gene signatures were derived from colonic epithelial cells and not from contaminating lymphocytes, RAG1 KO mice deficient in intraepithelial lymphocytes were used. Results: The analysis of differential expressed genes of colonic epithelial cells revealed multiple effects of dietary cellulose on the transcriptional profiles. In addition, cellulose caused a distinct clustering when comparing signature genes of different epithelial cell types. Conclusion: This study demonstrated that dietary cellulose impacts transcriptional programs in colonic epithelial cells during inflammation.
2021-05-31 | GSE151136 | GEO
Project description:Analysis of non-differentiated Caco-2 intestinal epithelial cell line treated with polydextrose fermentation metabolites fermented for 48 hours in 4-stage in vitro colon simulator, in which the conditions mimic the human proximal, ascending, transverse and distal colon in sequence , as well as with medium, 100 mM NaCl and 5 mM butyrate. Polydextrose, a soluble fiber fermented in colon, was fermented with the in vitro colon simulator in three amounts of 0%, 1% and 2%. Results provide insight into the mechanisms underlying colon cancer cells and a comparison of a complex fiber metabolome to 5 mM butyrate and 100 mM NaCl. Furthermore, the results give insight of dosage effect of increasing the concentration of fiber. High level of dietary fiber has been epidemiologically linked to protection against the risk for developing colon cancer. The mechanisms of this protection are not clear. Fermentation of dietary fiber in the colon results in production of for example butyrate that has drawn attention as a chemopreventive agent. Polydextrose, a soluble fiber that is only partially fermented in colon, was fermented in an in vitro colon simulator, in which the conditions mimic the human proximal, ascending, transverse and distal colon in sequence. The subsequent fermentation metabolome were applied on colon cancer cells, and the gene expression changes studied. Polydextrose fermentation down-regulated classes linked with cell cycle, and affected number of metabolically active cells. Further, up-regulated effects on classes linked with apoptosis implicate that polydextrose fermentation plays a role in induction of apoptosis in colon cancer cells. The up-regulated genes involved also key regulators of lipid metabolism, such as PPARg and PGC-1α. These results offer hypotheses for the mechanisms of two health benefits linked with consumption of dietary fiber, reducing risk of development of colon cancer, and dyslipidemia.
2011-04-22 | GSE28792 | GEO
Project description:Analysis of non-differentiated Caco-2 intestinal epithelial cell line treated with polydextrose fermentation metabolites fermented for 48 hours in 4-stage in vitro colon simulator, in which the conditions mimic the human proximal, ascending, transverse and distal colon in sequence , as well as with medium, 100 mM NaCl and 5 mM butyrate. Polydextrose, a soluble fiber fermented in colon, was fermented with the in vitro colon simulator in three amounts of 0%, 1% and 2%. Results provide insight into the mechanisms underlying colon cancer cells and a comparison of a complex fiber metabolome to 5 mM butyrate and 100 mM NaCl. Furthermore, the results give insight of dosage effect of increasing the concentration of fiber. High level of dietary fiber has been epidemiologically linked to protection against the risk for developing colon cancer. The mechanisms of this protection are not clear. Fermentation of dietary fiber in the colon results in production of for example butyrate that has drawn attention as a chemopreventive agent. Polydextrose, a soluble fiber that is only partially fermented in colon, was fermented in an in vitro colon simulator, in which the conditions mimic the human proximal, ascending, transverse and distal colon in sequence. The subsequent fermentation metabolome were applied on colon cancer cells, and the gene expression changes studied. Polydextrose fermentation down-regulated classes linked with cell cycle, and affected number of metabolically active cells. Further, up-regulated effects on classes linked with apoptosis implicate that polydextrose fermentation plays a role in induction of apoptosis in colon cancer cells. The up-regulated genes involved also key regulators of lipid metabolism, such as PPARg and PGC-1α. These results offer hypotheses for the mechanisms of two health benefits linked with consumption of dietary fiber, reducing risk of development of colon cancer, and dyslipidemia. Non-differentiated Caco-2 cells were treated with polydextrose fermentation metabolites from the vessels representing different parts of the colon, or with 100 mM NaCl or with 5 mM butyrate for 24 hours. For polydextrose fermentation three concentrations of polydextrose were used: 0%, 1% and 2% for a simulation that lasted for 48 hours. Polydextrose fermentation samples from total of 12 vessels, as well as from medium sample, 5 mM butyrate and 100 mM NaCl were analysed as single replica.
2011-04-22 | E-GEOD-28792 | biostudies-arrayexpress