Characterisation of the sensory phenotype of the oesophageal mucosa in gastroesophageal reflux disease
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PROVIDER: PRJNA939567 | ENA |
REPOSITORIES: ENA
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Project description:Identification of Novel Immune Cell Signature in Gastroesophageal Reflux Disease: Altered Mucosal Mast Cells and Dendritic Cell Profile. The mechanisms underlying the most troublesome symptom of gastroesophageal reflux disease (GERD), heartburn, remain incompletely understood. The pathogenesis of heartburn in GERD is likely to involve not only central mechanisms of sensitization including hypervigilance, but also multiple mucosal factors including maintenance of epithelial barrier integrity via tight junction proteins, expression of acid-sensing ion channels on nerve endings, and mucosal inflammation . We hypothesized that immune cell components play a regulatory role in mucosal mechanisms of sensitization in GERD, and aimed to identify differences in the immune cell signature and sensory mucosal markers between reflux phenotypes and healthy asymptomatic subjects.
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Project description:Transcriptional profiling of adult esophageal epithelium comparing wild-type mice with Nrf2-/- mice with or without gastroesophageal reflux for 4 weeks. Goal was to determine the role of Nrf2 on the barrier function of mouse esophageal epithelium. Two-class comparisons. Wild-type/without reflux vs. Nrf2-/-/without reflux; Wild-type/gastric reflux vs. Nrf2-/-/gastric reflux; Wild-type/duodenal reflux vs. Nrf2-/-/duodenal reflux; Wild-type/mixed reflux vs. Nrf2-/-/mixed reflux. Biological replicates: 3 replicates for each group.
2013-01-01 | E-GEOD-39629 | biostudies-arrayexpress
Project description:Oesophageal exposure to duodenogastroesophageal refluxate is implicated in the development of Barrett’s Metaplasia, with increased risk of progression to oesophageal adenocarcinoma. The literature proposes that reflux exposure activates NF-kB, driving the aberrant expression of intestine-specific caudal-related homeobox genes. However, early events in the pathogenesis of Barrett’s Metaplasia from a normal epithelium are poorly understood. To investigate this, our study subjected a 3D model of the normal human oesophageal mucosa to repeated, pulsatile exposure to specific bile components and examined changes in gene expression. Initial 2D experiments with a range of bile salts observed that taurochenodeoxycholate (TCDC) impacted upon NF-kB activation without causing cell death. Informed by this, the 3D human oesophageal model was repeatedly exposed to TCDC in the presence and absence of acid, and the epithelial cells underwent gene expression profiling. We identified ~300 differentially expressed genes following each treatment, with a large and significant overlap between treatments. Enrichment analysis (Broad GSEA, DAVID and Metacore™, GeneGo Inc) identified multiple gene sets related to cell signalling, inflammation, proliferation, differentiation and cell adhesion. Specifically NF-kB activation, Wnt signalling, cell adhesion and targets for the transcription factors PTF1A and HNF4α were highlighted. CDX1/2 transcription factors are believed to play a role in BM development; however, in this study their targets were not enriched, suggesting that CDX1/2 activation may not be the one of the initial events for BM formation. Our findings highlight new areas for investigation in the earliest stages of BM pathogenesis of oesophageal diseases and new potential therapeutic targets.
2013-03-22 | GSE45380 | GEO
Project description:Transcriptional profiling of adult esophageal epithelium comparing wild-type mice with Nrf2-/- mice with or without gastroesophageal reflux for 4 weeks. Goal was to determine the role of Nrf2 on the barrier function of mouse esophageal epithelium.
2013-01-01 | GSE39629 | GEO
Project description:Oesophageal exposure to duodenogastroesophageal refluxate is implicated in the development of BarrettM-bM-^@M-^Ys Metaplasia, with increased risk of progression to oesophageal adenocarcinoma. The literature proposes that reflux exposure activates NF-kB, driving the aberrant expression of intestine-specific caudal-related homeobox genes. However, early events in the pathogenesis of BarrettM-bM-^@M-^Ys Metaplasia from a normal epithelium are poorly understood. To investigate this, our study subjected a 3D model of the normal human oesophageal mucosa to repeated, pulsatile exposure to specific bile components and examined changes in gene expression. Initial 2D experiments with a range of bile salts observed that taurochenodeoxycholate (TCDC) impacted upon NF-kB activation without causing cell death. Informed by this, the 3D human oesophageal model was repeatedly exposed to TCDC in the presence and absence of acid, and the epithelial cells underwent gene expression profiling. We identified ~300 differentially expressed genes following each treatment, with a large and significant overlap between treatments. Enrichment analysis (Broad GSEA, DAVID and MetacoreM-bM-^DM-", GeneGo Inc) identified multiple gene sets related to cell signalling, inflammation, proliferation, differentiation and cell adhesion. Specifically NF-kB activation, Wnt signalling, cell adhesion and targets for the transcription factors PTF1A and HNF4M-NM-1 were highlighted. CDX1/2 transcription factors are believed to play a role in BM development; however, in this study their targets were not enriched, suggesting that CDX1/2 activation may not be the one of the initial events for BM formation. Our findings highlight new areas for investigation in the earliest stages of BM pathogenesis of oesophageal diseases and new potential therapeutic targets. RNA was extracted from oesophageal epithelium grown in a 3D oesophageal mucosa model. The model received pulsatile exposure for 10 mins twice a day for 11 days to pH 7.4 (control, n=6), TCDC (n=6), pH 4 (n=6) or TCDC, pH 4 (n=6). In one experiment, four oesophageal constructs were grown using the epithelial cells from one patient and each construct was exposed to a different insult. The experiment was performed six times using cells from three different patients, repeating each experiment once to produce technical replicates. RNA was then pooled from one technical replicate per patient to produce 8 samples for array analysis. The three treatments were compared to the control.
2013-03-22 | E-GEOD-45380 | biostudies-arrayexpress
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2021-12-01 | GSE182974 | GEO
Project description:Differential gene expression analysis of oesophageal cells stimulated with a low pH environment. Study designed to identify pathways involved in progression of gastro-oesophageal reflux disease through Barrett's oesophagus to adenocarcinoma. Identified many subsets of genes with involvement in pathogenesis. Keywords = GORD Keywords = Barrett's Oesophagus Keywords = Oesopageal Adenocarcinoma. Keywords: time-course
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Project description:Saliva is the most important biological factor to protect against erosive tooth wear (ETW). Gastroesophageal reflux disease (GERD) patients have an increased risk of ETW due to the frequent presence of intrinsic acids in the oral cavity. Remarkably, not all GERD patients suffer from ETW, which might be due to differences in the composition of the saliva.
2022-01-19 | PXD030712 | Pride
Project description:The gut and local esophageal microbiome progressively shift from healthy commensal bacteria to inflammatory-linked pathogenic bacteria in patients with gastroesophageal reflux disease, Barrett’s esophagus and esophageal adenocarcinoma (EAC). However, mechanisms by which microbial communities contribute to reflux-driven EAC remain incompletely understood and challenging to target. Herein, we utilized a rat reflux-induced EAC model to investigate targeting the gut microbiome-esophageal metabolome axis with cranberry proanthocyanidins (C-PAC) to inhibit EAC progression. Sprague Dawley rats, with or without reflux-induction received water or C-PAC ad libitum (700 µg/rat/day) for 25 or 40 weeks. C-PAC exerted prebiotic activity abrogating reflux-induced dysbiosis, and mitigating bile acid metabolism and transport, culminating in significant inhibition of EAC through TLR/NF-κB/TP53 signaling cascades. At the species level, C-PAC mitigated reflux-induced pathogenic bacteria (Streptococcus parasanguinis, Escherichia coli, and Proteus mirabilis). C-PAC specifically reversed reflux-induced bacterial, inflammatory and immune-implicated proteins and genes including Ccl4, Cd14, Crp, Cxcl1, Il6, Il1β, Lbp, Lcn2, Myd88, Nfkb1, Tlr2 and Tlr4 aligning with changes in human EAC progression, as confirmed through public databases. C-PAC is a safe promising dietary constituent that may be utilized alone or potentially as an adjuvant to current therapies to prevent EAC progression through ameliorating reflux-induced dysbiosis, inflammation and cellular damage.
2024-02-08 | GSE254633 | GEO
Project description:Differential gene expression analysis of oesophageal cells stimulated with a low pH environment. Study designed to identify pathways involved in progression of gastro-oesophageal reflux disease through Barrett's oesophagus to adenocarcinoma. Identified many subsets of genes with involvement in pathogenesis.<br><br>Missing data files: GSM38763.CEL (Time 0 mins rep 1), GSM38764.CEL (Time 0 mins rep 2), GSM38771.CEL (Time 240 mins rep 1), and GSM38772.CEL (Time 240 mins rep 2).
2007-08-25 | E-GEOD-2144 | biostudies-arrayexpress