Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microarray analysis of long noncoding RNA expression profile in HeLa cells infected Chlamydia trachomatis

ABSTRACT: Chlamydia trachomatis (C. trachomatis) is an intracellular bacterium, and is one of the main pathogens that cause sexually transmitted infections worldwide. Long non-coding RNAs (lncRNAs) have become vital regulators in many biological processes. However, few studies have shown that lncRNAs take part in the pathogenesis of C. trachomatis. Here, we used microarrays to study the expression profiles of lncRNAs and mRNAs in HeLa cells at 12, 24, and 40 hours pot-infection (hpi). Our study provides evidence that lncRNAs are involved in the interaction between C. trachomatis and hosts.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165628 | GEO | 2021/07/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide analysis of Chlamydia trachomatis-infected cells

Project description:Chlamydia trachomatis is the most common sexually transmitted infection and the bacterial agent of trachoma globally. C. trachomatis undergoes a biphasic developmental cycle involving an infectious elementary body and a replicative reticulate body. Little is currently known about the expression of host cell mRNAs, lncRNAs, and miRNAs at different stages of C. trachomatis development. Here, we performed RNA-seq and miR-seq on HeLa cells infected with C. trachomatis serovar E at 20 hpi and 44 hpi with or without IFN-γ treatment. Our study identified and validated differentially expressed host cell mRNAs, lncRNAs, and miRNAs during infection. Infection at 20 hpi showed the most differential upregulation of both coding and non-coding genes while infection at 44 hpi in the presence of IFN-γ resulted in a dramatic downregulation of a large proportion of genes. Using RT-qPCR, we validated the top 5 stage-specific upregulated mRNAs and miRNAs. One of the commonly expressed miRNAs at all three stages, miR-193b-5p, showed significant expression in clinical serum samples of C. trachomatis-infected patients as compared to sera from healthy controls and HIV-1-infected patients. Furthermore, at 20 hpi we observed significant upregulation of antigen processing and presentation, and T helper cell differentiation pathways whereas T cell receptor, mTOR, and Rap1 pathways were modulated at 44 hpi. Treatment with IFN-γ at 44 hpi showed the regulation of cytokine-cytokine receptor interaction, FoxO signaling, and Ras signaling pathways. Our study documents a role for the stage-specific transcriptional manipulation of the host cell genome and important signaling pathways that are necessary for the survival of pathogen and could serve as potential biomarkers in the diagnosis and management of the disease.

2021-01-13 | GSE158814 | GEO

Plasmid-free Chlamydia trachomatis elicit lowered inflammation, delayed apoptosis, and reduced chemoattractant expression in HeLa cells compared to plasmid-containing wild type

Project description:Chlamydia trachomatis serovariants are responsible for either Trachoma, the leading cause of infectious blindness or sexually transmitted disease, wherein the endocervix is the most frequently infected site in women. Disease caused by Chlamydia typically involves chronic inflammation and scarring. Recent work with a live-attenuated A2497 plasmid deficient vaccine strain (A2497-) demonstrated protection in nonhuman primates against trachoma and a lack of measurable ocular pathology in A2497- infected monkeys. We therefore performed host cell transcriptome analysis of Hela cells infected with A2497 plasmid-containing (A2497) and A2497- Chlamydia over time. Our results indicate that relative to wild type A2497, the A2497- variant illicits a transcriptome response indicative of lowered inflammation response a delayed apoptosis response, a reduction in immune cell recruitement cytokine expression and a reduction in genes involved in cell proliferation and or fibrosis-like activities. The data provided here suggests a model that may explain how plasmid deficient chlamydia may provide an immuno-protective response without the pathology normally seen with plasmid-containing bacteria. Ct infection with and without plasmid time series

2014-11-25 | E-GEOD-56168 | biostudies-arrayexpress

Differential expression of mRNA encoding cytokines and chemokines in the reproductive tract after infection of mice with Chlamydia trachomatis

Project description:Chlamydia trachomatis is an obligate intracellular pathogen and the most frequently reported sexually transmitted bacteria in the United States. Infection with Chlamydia trachomatis targets epithelial cells within the genital tract which respond by secreting chemokines and cytokines. Persistent inflammation can lead to fibrosis, tubal infertility and/or ectopic pregnancy. Our objective was to determine the inflammatory mediators involved in clearance of low-grade infection and the potential involvement in chronic inflammation. Our hypothesis was that mRNA encoding pro-inflammatory cytokines and chemokines will be differentially expressed in the female reproductive tract of mice infected with C. trachomatis at both 28 and 35 days post-infection compared to controls. Superarray analysis was performed using RT2 Profiler PCR arrays for mouse Cytokines and Chemokines (Qiagen).

2014-10-18 | GSE62461 | GEO

Expression data of A2EN cells during early stage of Chlamydia trachomatis infection

Project description:Chlamydia trachomatis is an obligate intracellular pathogen that causes trachoma and sextually transmitted disease in human. During early stage of infection, Chlamydia secreted bacterial effector proteins into host cell cytoplasm to help its entry and estabilishment of early replicated niche. We identified a Chlamydia mutant that lack an early Effector. To address the function of this effector, we infected A2EN cells with this mutant (G1V) and its complemented counterpart (G1TEPP) to see what host gene transcriptions are affected by this effector. A2EN cells were mock infected, or infected with a Chlamydia mutant or its complemented counterpart for 4 hour post infection.

2014-04-09 | E-GEOD-54336 | biostudies-arrayexpress

Plasmid-free Chlamydia trachomatis elicit lowered inflammation, delayed apoptosis, and reduced chemoattractant expression in HeLa cells compared to plasmid-containing wild type

2014-11-25 | GSE56168 | GEO

Expression data of A2EN cells during early stage of Chlamydia trachomatis infection

2014-04-09 | GSE54336 | GEO

Exploiting induced pluripotent stem cell-derived macrophages to unravel host factors influencing Chlamydia trachomatis pathogenesis

Project description:Chlamydia trachomatis remains a leading cause of bacterial sexually transmitted infections and preventable blindness worldwide. There are, however, limited in vitro models to study the role of host genetics in the response of macrophages to this obligate human pathogen. Here, we describe an approach using macrophages derived from human induced pluripotent stem cells (iPSdMs) to study macrophage-Chlamydia interactions in vitro. We show that iPSdMs support the full infectious life cycle of C. trachomatis in a manner that mimicks the infection of human blood-derived macrophages. Transcriptomic and proteomic profiling of the macrophage response to chlamydial infection highlights the role of the type I interferon and interleukin 10-mediated responses. Using CRISPR/Cas9 technology, we generate biallelic knockout mutations in the host genes encoding IRF5 and IL-10RA in iPSCs, confirming their roles in limiting chlamydial infection in macrophages. This model can potentially be extended to other pathogens and tissue systems to advance our understanding of host-pathogen interactions and the role of human genetics in influencing the outcome of infections.

2018-02-14 | PXD005858 | Pride

Heat shock-induced transcriptomic response in Chlamydia trachomatis

Project description:Heat shock-induced transcriptomic response in Chlamydia trachomatis

2021-12-08 | GSE173366 | GEO

Chlamydia trachomatis induces the transcriptional activity of host YAP in a Hippo-independent fashion

Project description:The obligate intracellular pathogen Chlamydia trachomatis is the causative agent of the most common bacterial sexually transmitted disease worldwide. While the host response to infection by this pathogen has been well characterized, it remains unclear to what extent host gene expression during infection is the product of Chlamydia-directed modulation of host transcription factors. In this report, we show the transcriptome of Chlamydia-infected epithelial cells exhibits gene expression consistent with activity of YAP, a transcriptional coactivator implicated in cell proliferation, wound healing, and fibrosis. After confirming induction of YAP target genes during infection, we observed increased YAP nuclear translocation in Chlamydia-infected epithelial cells. We further show that increased YAP activation is a Chlamydia-directed process, requiring de novo protein synthesis during midcycle infection. Surprisingly, infection-mediated YAP activation bypasses YAP inhibition by the Hippo kinase cascade, with phosphorylation at S127 remaining unchanged. Instead, phosphorylation at Y357 was increased along with nuclear translocation, indicating that infection overrides phospho-inhibition at S127. Nuclear translocation of Y357F mutant YAP was not increased by infection, demonstrating that chlamydial YAP activation requires phosphorylation at this residue. Taken together, our results define a transcriptome-altering mechanism potentially linked to chlamydial fibrosis and other advanced disease sequelae.

2023-02-13 | GSE198272 | GEO

Chlamydia trachomatis induces the transcriptional activity of host YAP in a Hippo-independent fashion

2023-02-13 | GSE180782 | GEO