Ontology highlight
ABSTRACT:
PROVIDER: PRJNA564342 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10082176.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 1 of 1 |
Similar Datasets
Project description:Among the non-polio enterovirus (NPEV) Echovirus-30 (E-30) is responsible for extensive global outbreaks of meningitis in children. To gain access to the central nervous system (CNS), E-30 first have to cross one of the two main barriers, the epithelial blood-cerebrospinal fluid (CSF) barrier (BCSFB) or the endothelial blood-brain barrier (BBB). Previously it has been shown that several meningitis causing bacteria preferentially infect human choroid plexus papilloma cells (HIBCPP) in a polar fashion from the basolateral cell side. Here, we investigated the polar infection with E-30 of HIBCPP cells. Both, apical and basolateral infections caused a significant decrease of the transepithelial resistance (TEER) of HIBCPP cells in a dose-dependent manner. However, to reach the same TEER decrease the multiplicity of infection (MOI) of the apical infection had to be 20 times higher than the basolateral infection. In line with this finding the number of infected cells at respective time-points after basolateral infection was significantly higher compared to apical infection. Cytotoxic effects of E-30 on HIBCPP cells during basolateral infection were observed following prolonged infection, and appeared more drastically compared to the apical infection. Evaluation of massive analysis of cDNA ends (MACE) RNA data comparing basolateral versus apical infection, revealed a distinct pattern of up- and down-regulated genes depending on the side of infection. Especially, the down-regulation of ITGα5 upon basolateral infection can be correlated with a more drastic impact of E-30 on the HIBCPP cells when compared to apical infection, leading to structural changes. Also, type 3 interferon genes might be a factor involved in the polar effect of E-30 on HIBCPP. Altogether, the data highlights the polar effect of E-30 in HIBCPP cells as an important factor for an efficient infection.
2020-10-02 | GSE146890 | GEO
Project description:Echovirus-30 (E-30) is a non-polio enterovirus responsible for meningitis outbreaks in
children worldwide. To gain access to the central nervous system (CNS), E-30 first has to cross the
blood-brain barrier (BBB) or the blood-cerebrospinal fluid barrier (BCSFB). E-30 may use lipid rafts of
the host cells to interact with and to invade the BCSFB. To study enteroviral infection of the BCSFB,
an established in vitro model based on human immortalized brain choroid plexus papilloma (HIBCPP)
cells has been used. Here, we investigated the impact of E-30 infection on the protein content of
the lipid rafts at the BCSFB in vitro. Mass spectrometry analysis following E-30 infection versus
uninfected conditions revealed differential abundancy in proteins implicated in cellular adhesion,
cytoskeleton remodeling, and endocytosis/vesicle budding. Further, we evaluated the blocking of
endocytosis via clathrin/dynamin blocking and its consequences for E-30 induced barrier disruption.
Interestingly, blocking of endocytosis had no impact on the capacity of E-30 to induce loss of barrier
properties in HIBCPP cells. Altogether, these data highlight the impact of E-30 on HIBCPP cells
microdomain as an important factor for host cell alteration.
2020-12-29 | MSV000086646 | MassIVE
Project description:Increasing evidence has demonstrated that circular RNA exerts important function in the pathogenesis of some diseases. While, the contributions of circRNAs to aseptic lossening after total hip arthroplasty remain largely unknown. Our research is to explore the differently expressed circRNAs and elucidate complex regulated mechanism of circRNAs in aseptic lossening. The differently expressed circRNAs were identified by RNA sequencing analysis. Reverse transcription-quantitative polymerase chain reaction was adopted to corroborate these differently expressed circRNAs. The potential function of circRNAs in aseptic lossening tissue was identified by competing endogenous RNA analysis. Enrichment analysis were performed for target mRNAs and host genes of the differently expressed circRNAs by Gene Oncology and Kyoto Encyclopedia of Genes and Genomes. 257 differently expressed circRNAs were obtained from RNA-seq results. Then, circRNA–miRNA–mRNA network was established based on the validated circRNAs. The result of Gene Oncology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis suggested that the circRNAs were related with some biological functions and pathways of aseptic lossening. A novel pathogenesis and treatment strategy about aseptic lossening after total hip arthroplasty was revealed from our study of circRNA–miRNA–mRNA network.
2021-01-19 | GSE149315 | GEO
Project description:ABSTRACT: Viral aseptic meningitis is a neuroinflammatory condition that occurs when viruses gain access to the central nervous system (CNS) and induce inflammation. The blood-brain barrier (BBB) is comprised of brain endothelial cells (BECs) that stringently regulate the passage of molecules, toxins, and pathogens from the circulation into the CNS. Through their unique properties, such as complex tight junctions, reduced rates of endocytosis, expression of efflux transporters, and restricted expression of leukocyte adhesion molecules, the BBB is often able to limit pathogen entry into the brain; however, certain neurotropic pathogens, such as coxsackievirus B3 (CVB3) are able to infect the CNS. We have previously demonstrated that CVB3 can infect and disrupt induced pluripotent stem cell-derived brain-like endothelial cells (iBECs), but the host response to this infection remains unknown. Here, we investigate global host transcriptional changes during CVB3 infection of iBECs using RNA sequencing. We validated our data set by exploring pathways altered by CVB3 using quantitative real-time PCR (qPCR) and enzyme-linked immunosorbent assay of upregulated cytokines and interferon signaling molecules. IMPORTANCE: Coxsackievirus B3 (CVB3) is a leading cause of viral aseptic meningitis that can cause severe disease in susceptible individuals. To gain access to the central nervous system, CVB3 must cross central nervous system barriers, such as the blood-brain barrier. Previously, we have shown that CVB3 infects a human stem cell-derived brain-like endothelial cell model. Here, we report the global transcriptome of stem cell-derived brain-like endothelial cells to CVB3 infection and provide proof-of-concept validation of the dataset using molecular biology techniques. These data could inform novel mechanisms of CVB3-mediated blood-brain barrier dysfunction. KEYWORDS: Coxsackievirus B3, blood-brain barrier, brain endothelial cells, RNA sequencing, induced pluripotent stem cells
2024-11-21 | GSE269413 | GEO
Project description:Cronobacter (C.) is an important emerging opportunistic foodborne pathogen representing significant cause of mortality in neonatal patients with bacteremia and meningitis. Knowledge on the pathobiology of Cronobacter mediated meningitis has to a large extend been explored using in vitro models. To explore the innate immune response against the neonatal sepsis/meningitis causing isolate C. turicensis z3032 in vivo, zebrafish larvae (Danio rerio) were used as infection model. Following establishment of infection in zebrafish larvae with z3032, dual RNA-sequencing of host-pathogen was undertaken to profile RNA expression simultaneously in the pathogen and the head region of the zebrafish host.
2024-06-28 | GSE236313 | GEO
Project description:Neutrophils are crucial mediators of host defense and are recruited to the central nervous system in large numbers during acute bacterial meningitis caused by S. pneumoniae. Neutrophils can release neutrophil extracellular traps (NETs) during infections to trap and kill bacteria. Intact NETs are fibrous structures and mainly consist of decondensed DNA and neutrophil-derived antimicrobial proteins. We report the extensive presence of NETs in the cerebrospinal fluid of patients with pneumococcal meningitis, and absence of NETs in other forms of meningitis caused by viruses, Borrelia and subarachnoid hemorrhage. In a rat model of meningitis, a clinical strain of pneumococci induced NET formation in the cerebrospinal fluid. Importantly, disrupting NETs using DNase I significantly reduced bacterial load, demonstrating that NETs contribute to the pathogenesis of pneumococcal meningitis in vivo. Targeting NETs using DNase may represent a novel indication for an already approved drug as a non-antibiotic therapeutic option to treat acute pneumococcal meningitis.
2019-11-12 | PXD011546 | Pride