Ontology highlight
ABSTRACT:
PROVIDER: PRJNA608537 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11179200_1.fastq.gz | Fastqsanger.gz | |||
| SRR11179200_2.fastq.gz | Fastqsanger.gz | |||
| SRR11179201_1.fastq.gz | Fastqsanger.gz | |||
| SRR11179201_2.fastq.gz | Fastqsanger.gz | |||
| SRR11179202_1.fastq.gz | Fastqsanger.gz |
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Project description:Ultra-Processed Foods drive Intestinal Barrier permeability increasing Microvascular Disease risk
| PRJNA596437 | ENA
Project description:Abstract: Our intake of ultra-processed foods has dramatically increased over the past few decades in line with the prevalence of obesity and diabetes, key risk factors for microvascular diseases such as chronic kidney disease (CKD). The extent to which long-term intake of highly processed food influences CKD outcome is unclear. Here, we show in rodent models that a highly processed diet drives intestinal barrier permeability and an increased risk of CKD. Inhibition of the advanced glycation pathway, which generates Maillard reaction products within foods upon thermal processing, reversed kidney injury. Consequently, a highly processed diet leads to innate immune complement activation and local kidney inflammation via the potent proinflammatory effector molecule complement 5a (C5a). C5a receptor inhibition ameliorated albuminuria. In a mouse model of diabetes, a high resistant starch fiber diet led to a redistribution of the gut commensal consortium, prevented impaired gut barrier function and decreased the severity of kidney injury via suppression of complement. These results provide mechanistic insight into the role of highly processed foods on inflammation and chronic disease risk. One Sentence Summary: Ultra-processed diets promote chronic kidney disease
2020-12-18 | GSE142261 | GEO
Project description:To study the role of RNF213, we generated RNF213-deficient human cerebral microvascular endothelial cells by the CRISPR-Cas9 double nickase method and showed that RNF213 may be an important regulator of the blood-brain barrier permeability and homeostasis
2021-09-08 | GSE183603 | GEO
Project description:Carotenoids are naturally occurring pigments in plants responsible for the orange, yellow, and red color of fruits and vegetables. Carrots are one of the primary dietary sources of carotenoids. The biological activities of carotenoids in higher organisms are well documented in most tissues but not the large intestine. The gastrointestinal barrier acts as a line of defense against the systemic invasion of pathogenic bacteria, especially at the colonic level. Proteins involved in tight junction assembly between epithelial cells and mucus secretion from goblet cells are essential for maintaining intestinal barrier homeostasis. A high-fat diet can cause gut impairment by inducing barrier permeability, leading to low-grade chronic inflammation via metabolic endotoxemia. Our hypothesis for this study is that the dietary intake of carotenoid-rich foods can alleviate obesity-associated gut inflammation and strengthen the intestinal barrier function. Male C57BL/6J mice were randomized to one of four experimental diets for 20 weeks (n = 20 animals/group): Low-fat diet (LFD, 10% calories from fat), high-fat diet (HFD, 45% calories from fat), HFD with white carrot powder (HFD + WC), or HFD with orange carrot powder (HFD + OC). Colon tissues were harvested to analyze the biochemical effects of carotenoids in carrots. The distal sections were subjected to isobaric labeling-based quantitative proteomics in which tryptic peptides were labeled with tandem mass tags, followed by fractionation and LC-MS/MS analysis in an Orbitrap Eclipse Tribrid instrument. High-performance liquid chromatography results depicted that the HFD+WC pellets were carotenoid-deficient, and the HFD+OC pellets contained high concentrations of provitamin A carotenoids, specifically α-carotene and β-carotene. As a result of the quantitative proteomics, a total of 4410 differentially expressed proteins were identified. Intestinal barrier-associated proteins were highly upregulated in the HFD+OC group, particularly mucin-2 (MUC-2). Upon closer investigation into mucosal activity, other proteins related to MUC-2 functionality and tight junction management were upregulated by the HFD+OC dietary intervention. Carotenoid-rich foods may prevent high-fat diet-induced intestinal barrier disruption by promoting colonic mucus synthesis and secretion in mammalian organisms.
2024-11-04 | PXD054150 | Pride
Project description:Modern lifestyle is associated with a major consumption of ultra-processed foods (UPF) due to their practicality and palatability. The ingestion of emulsifiers, a main additive in UPFs, has been related to gut inflammation, microbiota dysbiosis, adiposity and obesity. Maternal unbalanced nutritional habits during embryonic and perinatal stages perturb offspring’s long-term metabolic health, thus increasing obesity and associated comorbidity risk. However, whether maternal emulsifier consumption influences developmental programming in the offspring remains unknown. Here we show that, in mice, maternal consumption of dietary emulsifiers (1% CMC and 1% P80 in drinking water), during gestation and lactation, perturbs the development of hypothalamic energy balance regulation centers of the progeny, leads to metabolic impairments, cognition deficits and induces anxiety-like traits in a sex-specific manner. Our findings support the notion that maternal consumption of emulsifiers, common additives of UPFs, causes mild metabolic and neuropsychological malprogramming in the progeny. Our data call for nutritional advice during gestation.
2023-07-31 | GSE231769 | GEO
Project description:Background and Objectives: Antibiotic (ABx) therapy is associated with an increased risk for Crohn´s Disease but the underlying mechanisms are unknown. We observed high fecal serine protease activity (PA) to be a frequent side effect of ABx therapy in patients. The aim of the present study was to unravel whether this rise in PA may promote colitis development via detrimental effects on the large intestinal barrier. Design: Transwell experiments were used to assess the impact of high PA in ABx-treated patients or vancomycin/metronidazole (V/M)-treated mice on the epithelial barrier. Serine protease profiling was performed using LC-MS/MS analysis. The impact of high PA on the intestinal barrier in WT/IL10-/- mice and on colitis development in IL10-/- mice was investigated using V/M+/-oral serine protease inhibitor (AEBSF) treatment. Results: The ABx-induced high PA was found to be due to significantly increased levels of pancreatic proteases and to impair the epithelial barrier. In WT mice, the rise in PA caused a transient increase in intestinal permeability but did not affect susceptibility towards DSS-induced acute colitis. In IL10-/- mice, the rise in PA caused a lasting impairment of the intestinal barrier, which was associated with inflammatory activation of the large intestinal tissue. In the long term, the lasting increase in PA upon repeated V/M treatment aggravated colitis development in IL10-/-mice. Conclusion: High PA is a frequent adverse effect of ABx therapy which is detrimental to the large intestinal barrier and may contribute to the development of chronic inflammation in genetically susceptible individuals.
2018-05-11 | PXD007914 | Pride
Project description:The precise regulation of blood-brain-barrier (BBB) permeability for immune cells and blood-borne substances is essential to maintain brain homeostasis. Sphingosine-1-phosphate (S1P), a lipid signaling molecule enriched in plasma, is known to affect BBB permeability. Previous studies focussed on endothelial S1P receptors 1 and 2, reporting a barrier-protective effect of S1P1 and a barrier-disruptive effect of S1P2. Here we present novel data characterizing the expression, localization and function of the hitherto exclusively immunce cell-associated S1P receptor 4 (S1P4) on primary brain microvascular endothelial cells (BMECs). We detected a robust expression of S1P4 in homeostatic BMECs and pinpointed its localization to abluminal endothelial membranes by electron microscopy. Basolateral S1P treatment of BMECs led to increased permeability in vitro associated with S1P4 downregulation. Likewise, downregulation of S1P4 was observed in mouse brain microvessels after stroke, a neurological disease associated with BBB impairment. RNA sequencing analysis of BMECs suggested involvement of S1P4 in endothelial homeostasis, apicobasal polarity and barrier function. Using siRNA, pharmacological agonists and antagonists of S1P4 both in vitro and in vivo, we demonstrate a barrier-protective function of S1P4. We therefore suggest S1P4 as a novel target regulating BBB permeability and propose its therapeutic targeting in CNS diseases associated with BBB dysfunction.
2021-10-04 | GSE163561 | GEO
Project description:The effect of neuronal activity on blood-brain barrier function and whether it plays a role in plasticity in the healthy brain remains unclear. We show that neuronal activity induces modulation of microvascular permeability in the healthy brain and that it has a role in local network reorganization. Combining simultaneous electrophysiological recording and vascular imaging with transcriptomic analysis in rats, and functional and BBB-mapping MRI in human subjects we show that prolonged stimulation of the limb induces a focal increase in BBB permeability in the corresponding somatosensory cortex that is associated with long-term synaptic plasticity. We further show that the increased microvascular permeability depends on neuronal activity and involves caveolae-mediated transcytosis and transforming growth factor beta signaling. Our results reveal a role of BBB modulation in cortical plasticity in the healthy brain, highlighting the importance of neurovascular interactions for sensory experience and learning.
2024-01-31 | GSE223282 | GEO
Project description:Inflammatory bowel disease (IBD) patients exhibit compromised intestinal barrier function, enhanced inflammation, and increased cancer risk, with symptoms sometimes being exacerbated in women during pregnancy. To investigate the IBD phenotype and disease progression in human intestine, we leveraged organ-on-a-chip (Organ Chip) technology to engineer human Colon Chips lined by homotypic or heterotypic recombinants of intestinal epithelium interfaced with stromal fibroblasts isolated from Healthy or IBD patient-derived colon resections. Chips created with both epithelial and stromal cells from the same ulcerative colitis or Crohn's disease patient showed increased IBD-associated gene pathway activation, elevated pro-inflammatory cytokines, reduced mucus layer thickness, increased intestinal barrier permeability, compared to homotypic Healthy Colon Chips. When heterotypic tissue recombinants were created, the IBD stromal fibroblasts induced the IBD phenotype in healthy epithelium, and healthy colonic fibroblasts partially reduced inflammation in the IBD epithelium. Using this system, we discovered that peristalsis-like mechanical deformations directly impact colon tissue physiology by increasing mucin gene expression, mucus thickness, and barrier permeability in both Healthy and IBD Chips, and that they only stimulate a fibrotic response in IBD Chips. We also found that both inflammation and fibrosis were accentuated in IBD Chips created with cells from a female patient that were exposed to pregnancy-associated hormones. Interestingly, exposure to a carcinogen (N-ethyl-N-nitrosourea) for 3 weeks in vitro induced histological changes and gene duplication in the IBD Chips, but not in the Healthy Chips. These data suggest that the stroma plays a key role in driving inflammation and disease progression in IBD patients and that human Organ Chip technology may represent a new preclinical tool to gain insight into these mechanisms as well as to identify novel diagnostic biomarkers and therapeutics.
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Project description:The ERC “MINERVA” project (GA 724734) aims at developing a multi-organ-on-a-chip engineered platform to recapitulate in vitro the main players involved in the MGBA crosstalk: the microbiota, the gut epithelium, the immune system, the blood-brain barrier and the brain. In this context, the gut epithelium represents a physiological barrier that separates the intestinal lumen from the systemic circulation, and in several pathological circumstances, seems that its permeability might significantly increase and allow the passage of biologically active molecules into the blood vessels surrounding the intestinal mucosa. In the present work, we present our MINERVA 2.0 device and our innovative gut-on-a-chip device obtained by culturing in MINERVA 2.0 and a human gut epithelial CaCo2 cell based model. In particular, we have cultured the cells under perfusion and have assessed cell behavior by addressing cellular viability, tight junction imaging, apparent permeability by FITC-Dextran and transepithelial electrical resistance evaluation. Transcriptomic profile was used to further elucidate the effects of dynamic perfusion on Caco-2 cells.
2022-10-31 | E-MTAB-11949 | biostudies-arrayexpress