Ontology highlight
ABSTRACT:
PROVIDER: PRJNA823848 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18651809.fastq.gz | Fastqsanger.gz | |||
| SRR18651810.fastq.gz | Fastqsanger.gz | |||
| SRR18651811.fastq.gz | Fastqsanger.gz | |||
| SRR18651812.fastq.gz | Fastqsanger.gz | |||
| SRR18651813.fastq.gz | Fastqsanger.gz |
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Project description:The hypothesis of this research was that probiotic bacteria that increase intestinal barrier function achieve this, partly, by increasing the expression of the genes involved in tight junction signalling in healthy intestinal epithelial cells. L. plantarum MB452 isolated from the probiotic product VSL#3 was chosen as the test bacterium because it has a robust, repeatable, positive effect tight junction integrity, as measured by the trans-epithelial electrical resistance (TEER) in vitro.
2009-10-07 | GSE18372 | GEO
Project description:Type III interferons (IFNλs) play crucial roles in antiviral defense and intestinal epithelial barrier integrity. While interferon expression has been primarily studied in response to pathogens, basal interferon expression occurs in pathogen-free environments. However, the mechanisms regulating basal IFNλ expression and its function have not yet been elucidated. Our findings reveal that basal IFNλ2/3 expression correlates with the development of an intact cellular epithelium characterized by formation of tight junctions and establishment of barrier function. We discovered that basal IFNλ2/3 expression depends on cGAS/STING-mediated mitochondrial DNA detection and is inhibited by the Hippo mechanotransduction pathway at low cellular densities. Notably, cells lacking basal IFNλ2/3 fail to develop proper tight junctions and barrier function. Mechanistically, we found that IFNλ2/3 negatively regulates claudin-2 expression, thereby promoting barrier formation as cells become confluent. These results demonstrate a previously unknown function of basal IFNλs in regulating epithelial cell junction formation and highlight their importance not only during pathogen challenges but also in maintaining epithelial cell function under steady-state conditions.
2025-06-02 | GSE279172 | GEO
Project description:Use of hormonal contraceptives (HC) could alter the bacterial community, immune response and epithelial barrier integrity of the female genital tract (FGT) mucosal environment, leading to increased susceptibility to sexually transmitted infections (STIs), including HIV. Here, we tested whether use of three types of HCs, injectable Net-En, combined oral contraceptives (COC) and NuvaRing, a combined contraceptive vaginal ring (CCVR), led to distinct patterns in FGT host transcriptomics transcriptome in South African adolescent females. In an intention-to-treat analysis, we observed few changes in endocervical gene expression in the Net-En and COC groups. Relative to the COC and Net-En arms, samples from the CCVR arm had significant elevation of transcriptional networks driven by IL-6, IL-1 and NFKB, and lower expression of genes supporting epithelial barrier integrity. An integrated multivariate analysis of the cervicovaginal microbiome, transcriptome and cytokines demonstrated that networks of microbial dysbiosis and inflammation accurately discriminated the CCVR arm from the other contraceptive groups, while genes involved in epithelial cell differentiation were predictive of the Net-En and COC arms.
2022-07-11 | GSE171825 | GEO
Project description:The multiple toxic effects of Ochratoxin A(OTA) are a real threat for human beings and animal health. It has been suggested that probiotic improve the epithelial barrier disruption and reduce cell damage induced by mycotoxins. However, the exact effect and mechanism of probiotic Bacillus subtilis CW14 on epithelial barrier function is not well understood. The aim of this study was to examine whether B. subtilis CW14 could protect against OTA-induced barrier disruption and cell damage in human intestinal epithelial cell line (Caco-2). The results showed that OTA was absorbed efficiently in Caco-2 cells, led to microvilli disruption and tight junction protein(ZO-1 and claudin-1) damage, and suppressed cell proliferation by arresting cell cycle in G2/M phase and promoting apoptosis. The addictive of B. subtilis CW14 strains could partially reversed the tight junction injury by improving the ZO-1 protein expression and reduced the apoptosis induced by OTA. Furthermore, the transcriptome analysis data indicated that OTA mainly down-regulated the gene expression involved in tight junctions, cell cycle, and apoptosis-related signaling pathways. While the B. subtilis CW14 has the potential to protect epithelial barrier through activating the toll-like receptor signaling pathway, and could partially repair the OTA damage by down-regulating the TRAIL death receptor genes and up-regulating the DNA repair genes. Our findings suggest an important implication for the role of B. subtilis CW14 on the regulation of tight junction proteins and reduction cell death in intestine epithelial cells, and that is a potential candidate as a food additive to protect against intestinal damage.
2019-12-31 | GSE115081 | GEO
Project description:Dietary components and their metabolites produced by intestinal bacteria play a crucial role in maintaining intestinal epithelial integrity. Disrupted epithelial integrity can lead to increased permeability and chronic inflammation in the colon, known as ulcerative colitis (UC), in genetically predisposed individuals. Our data identified 3-aminobenzoic acid (3-ABA) as a key metabolite that reduces epithelial permeability and enhances barrier integrity in Caco2 cells by modulating the tight junctional regulatory pathway. Attenuated experimental colitis in mice treated with 3-ABA and decreased fecal 3-ABA in patients with UC implied the potential usefulness of 3-ABA as a novel treatment target for UC.
2025-05-01 | GSE270624 | GEO
Project description:The intestinal ecosystem is balanced by dynamic interactions between resident and incoming microbes, the gastrointestinal barrier, and the mucosal immune system. However, in the context of inflammatory bowel diseases (IBD) where the integrity of the gastrointestinal barrier is compromised, resident microbes contribute to the development and perpetuation of inflammation and disease. In this context, probiotic bacteria exert beneficial effects enhancing epithelial barrier integrity. However, the mechanisms underlying these beneficial effects are only poorly understood. Here, we comparatively investigated the effects of four probiotic lactobacilli, namely L. acidophilus, L. fermentum, L. gasseri, and L. rhamnosus in a T84 cell epithelial barrier model. Results of DNA-microarray experiments indicating that lactobacilli modulate the regulation of genes encoding in particular adherence junction proteins such as E-cadherin and b-catenin were confirmed by qRT-PCR. Furthermore, we show that epithelial barrier function is modulated by Gram-positive probiotic lactobacilli via their effect on adherence junction protein expression and complex formation. In addition, incubation with lactobacilli differentially influences the phosphorylation of adherence junction proteins and of PKC isoforms such as PKCd which thereby positively modulates epithelial barrier function. Further insight into the underlying molecular mechanisms triggered by these probiotics might also foster the development of novel strategies for the treatment of gastrointestinal diseases (e.g. IBD).
2012-02-10 | E-MEXP-3445 | biostudies-arrayexpress
Project description:Colonic epithelial cells facilitate host-microbe interactions to control mucosal immunity, and they also coordinate recycling and forming the mucus barrier. Epithelial barrier breakdown underpins inflammatory bowel disease (IBD). However, we do not know the specific contributions of each epithelial cell subtype to this process. Here, we profiled single colonic epithelial cells in health and IBD. Our results identified previously unknown subtypes and crypt gradients of progenitors, colonocytes and goblet cells. We also revealed a novel specialized metal ion storage and chloride secretory cell. In IBD, we discovered a unique cluster of disease associated goblet cells that remodels the barrier. We found downregulated WFDC2, a novel goblet cell expressing anti-protease that inhibited bacterial growth. Our in vivo studies demonstrated WFDC2 preserved tight junction integrity and prevented commensal invasion and mucosal inflammation. We delineate markers and transcriptional states, identify a new colonic epithelial cell and uncover fundamental principles of epithelial plasticity and barrier breakdown in IBD. Thus, our study reveals new therapeutic targets and disease-related mechanisms in IBD
2019-02-16 | PXD011655 | Pride
Project description:Epithelium barrier integrity is assumed at least in part by the presence of junctions between cells. Tight-junction formation may be necessary for Sertoli cells to cease dividing and to support germ cell development. Microarray analysis of P20 Cldn11 +/- and Cldn11-/- testes confirmed the impact od Cldn11 deficiency on cell cytoskeleton and junction-related genes. Keywords: transcriptomic analysis
2010-04-11 | GSE15492 | GEO
Project description:Proliferative retinopathies are associated with abnormal angiogenesis that can result in visual impairment or vision loss. The tight junction complex regulates blood-retinal barrier integrity; however, its role in proliferative retinopathies is still at an early stage. Here, we employed human retinal endothelial cells (HRMVECs), and a mouse model of oxygen-induced retinopathy (OIR) to investigate the impact of IL-33 signaling on tight junction disintegration and pathological angiogenesis. Our experimental findings demonstrate that IL-33 induces ZO-1 serine/threonine phosphorylation and tight junction disruption in HRMVECs. In addition, mass-spectroscopy (MS) analysis revealed that treating of HRMVECs with IL-33 induces ZO-1 phosphorylation at Thr861 residue. Furthermore, we observed that NOX1-PKC- signaling modulates IL-33-induced ZO-1 phosphorylation and tight junction integrity in HRMVECs. We also observed that IL-33 depletion significantly reduces OIR-induced NOX1-PKC-ZO-1 signaling, vascular leakage, and pathological retinal neovascularization in the ischemic retina. We also observed that the NOX1-specific inhibitor, fluoflavine (ML-090), attenuated OIR-induced NADPH oxidase activity and pathological retinal neovascularization in the ischemic retina. Thus, we infer that IL-33-mediated NOX1-PKC-ZO-1 signaling regulates ischemia-induced retinal endothelial cell tight junction disruption and retinal neovascularization.
2025-10-14 | PXD060282 | Pride
Project description:Epithelium barrier integrity is assumed at least in part by the presence of junctions between cells. Tight-junction formation may be necessary for Sertoli cells to cease dividing and to support germ cell development. Microarray analysis of P20 Cldn11 +/- and Cldn11-/- testes confirmed the impact od Cldn11 deficiency on cell cytoskeleton and junction-related genes. Keywords: transcriptomic analysis Two-condition experiment: P20 Cldn11 +/- vs. P20 Cldn11 -/- testes. A pool of RNA from P20 Cldn11 +/- group was used as the reference group. Each P20 Cldn11 -/- was compared to reference group. Three biological replicates were processed in dye swap.
2010-04-11 | E-GEOD-15492 | biostudies-arrayexpress