Ontology highlight
ABSTRACT:
PROVIDER: PRJNA509676 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8304980_1.fastq.gz | Fastqsanger.gz | |||
| SRR8304980_2.fastq.gz | Fastqsanger.gz | |||
| SRR8304990_1.fastq.gz | Fastqsanger.gz | |||
| SRR8304990_2.fastq.gz | Fastqsanger.gz | |||
| SRR8305000_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 988 |
Similar Datasets
Project description:Chlamydia trachomatis is an obligate intracellular Gram-negative bacterium that frequently causes an asymptomatic genital tract infection, gradually cleared by host immunity Transcriptome profiles were made of endometrial tissue from women with or without genital tract C. trachomatis infection, to characterize host responses to infection. Profiles showed that infection polarized host defense toward Type 2 immune responses. Responses included fibrin deposition, enhanced wound repair, and tissue remodeling. Trans-cervical endometrial biopsy specimens were collected from 10 women with no identified upper or lower genital tract infection and 12 women with C. trachomatis endometrial infection.
2013-03-01 | E-GEOD-41075 | biostudies-arrayexpress
Project description:Chlamydia trachomatis is an obligate intracellular Gram-negative bacterium that frequently causes an asymptomatic genital tract infection, gradually cleared by host immunity Transcriptome profiles were made of endometrial tissue from women with or without genital tract C. trachomatis infection, to characterize host responses to infection. Profiles showed that infection polarized host defense toward Type 2 immune responses. Responses included fibrin deposition, enhanced wound repair, and tissue remodeling.
2013-03-01 | GSE41075 | GEO
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
Project description:Chlamydia trachomatis is an obligate intracellular pathogen that replicates within a specialized membrane-bound compartment, the inclusion. Chlamydia species express a unique class of effectors, Incs, which are translocated from the bacteria by a Type III secretion system and are inserted into the inclusion membrane where they modulate the host-bacterium interface. C. trachomatis repositions specific host organelles during infection to acquire nutrients and evade host cell surveillance, however the bacterial and host proteins controlling these processes are largely unknown. Here, we identify an interaction between the host dynactin complex and the C. trachomatis Inc CT192 (CTL0444), hereafter named Dre1 for Dynactin Recruiting Effector 1. We show that dynactin is recruited to the inclusion in a Dre1-dependent manner and that inactivation of Dre1 diminishes the recruitment of specific host organelles, including the centrosome, mitotic spindle, and Golgi Apparatus to the inclusion. Inactivation of Dre1 results in decreased C. trachomatis fitness in cell-based assays and in a mouse model of infection. By targeting particular functions of the versatile host dynactin complex, Dre1 facilitates re-arrangement of certain organelles around the growing inclusion. Our work highlights how C. trachomatis employs a single effector to evoke specific, large-scale changes in host cell organization that establish the intracellular replicative niche without globally inhibiting host cellular function.
2025-03-31 | PXD028543 | Pride
Project description:Here we examined host cell gene expression in response to Chlamydia trachomatis infection by applying scRNA-Seq to in vitro C. trachomatis-infected HEp-2 epithelial cells and time-matched uninfected cells over the early chlamydial developmental cycle (3, 6 and 12 hours). We collected 264 single cells across both conditions all time points. The aims of the experiment were examining host cell responses to infection at single cell resolution, and identifying early host cell signatures of infection.
2019-11-19 | GSE132525 | GEO
Project description:We applied Formaldehyde-Assisted Isolation of Regulatory Elements enrichment followed by sequencing (FAIRE-Seq) to generate genome-wide temporal chromatin maps of Chlamydia trachomatis-infected human epithelial cells in vitro over the chlamydial developmental cycle. We detected both conserved and distinct temporal regions of chromatin accessibility associated with C. trachomatis infection. The observed differentially accessible chromatin regions, including several Clusters of Open Regulatory Elements (COREs) and temporally-enriched sets of transcription factors, may help shape the host cell response to infection. These regions and motifs were linked to genomic features and genes associated with immune responses, re-direction of host cell nutrients, intracellular signaling, cell-cell adhesion, extracellular matrix, metabolism and apoptosis. This work will serve as a basis for future functional studies of transcriptional regulation and epigenomic regulatory elements in Chlamydia-infected human cells.
2020-10-28 | GSE132448 | GEO
Project description:Chlamydia trachomatis is an important human pathogen that replicates inside the infected host cell in a unique vacuole, the inclusion. The formation of this intracellular bacterial niche is essential for productive Chlamydia infections. Despite its importance for Chlamydia biology, a holistic view on the protein composition of the inclusion, including its membrane, is currently missing. Here we describe a newly established method to purify inclusions from C. trachomatis infected epithelial cells and the analysis of the host cell-derived proteome by a combination of label free and stable isotope labeling -based quantitative proteomics. Computational analysis of the proteome data indicated that the inclusion is a complex intracellular trafficking platform that interacts with host cells' antero- and retrograde trafficking pathways. Furthermore, the inclusion is highly enriched for sorting nexins of the SNX-BAR retromer, a complex essential for retrograde trafficking. Functional studies showed that in particular SNX5 controls the C. trachomatis infection and that retrograde trafficking is essential for infectious progeny formation. In summary, our findings suggest that the inclusion of C. trachomatis is well embedded in the hosts' endomembrane system and hijacks retrograde trafficking pathways for effective infection.
2015-06-08 | PXD002113 | Pride
Project description:The obligate intracellular bacterium Chlamydia trachomatis replicates in a cytosolic vacuole in human epithelial cells. Infection of human cells with C. trachomatis causes substantial changes to many host cell signalling pathways but the molecular basis of such influence is not well understood. Studies of gene transcription of the infected cell have shown altered transcription of many host cell genes, indicating a transcriptional response of the host cell to the infection. We here describe that infection of human cells with C. trachomatis as well as infection of murine cells with C. muridarum profoundly inhibits protein synthesis of the infected host cell. This inhibition was accompanied by changes to the ribosomal profile of the infected cell indicative of a block of translation initiation, most likely as part of a stress response. The chlamydial protease CPAF also reduced protein synthesis in uninfected cells although CPAF-deficient C. trachomatis showed no defect in this respect. Analysis of polysomal mRNA as a proxy of actively transcribed mRNA identified a number of biological processes differentially affected by chlamydial infection. Mapping of differentially regulated genes onto a protein interaction network identified nodes of up- and down-regulated networks during chlamydial infection. Proteomic analysis of protein synthesis further suggested translational regulation of host cell functions by chlamydial infection. These results demonstrate reprogramming of the host cell during chlamydial infection through the alteration of protein synthesis.
2019-05-21 | GSE114556 | GEO
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.
2014-04-09 | GSE54336 | GEO
Project description:Chlamydia trachomatis are the etiological agents of a range of diseases and are epidemiologically associated with cervical and ovarian cancers. The interplay between host and chlamydia is highly complex, and to obtain panoramic view of the functional interplay, we performed combinatorial global phosphoproteomic and transcriptomic analyses of C. trachomatis-induced signaling. We identified numerous previously unknown C. trachomatis phosphoproteins and C. trachomatis-regulated host phosphoproteins that are substrates of kinases involved in various cellular processes. Interestingly, several host transcription factors (TFs) that are phosphorylated in C. trachomatis infections, including ETS2 repressor factor (ERF), proto-oncogenic transcription factor ETS1 are targets of ERK MAPK signaling. While these TFs were found to be essential for Chlamydia development, we demonstrated their involvement in inducing epithelial-to-mesenchymal transition in C. trachomatis infected cells by transcriptional regulation of genes involved in cellular motility and invasion. Our data reveals substantially unexplored complexity of C. trachomatis-induced signaling and provides broader insights into pro-carcinogenic potential of C. trachomatis.
2018-12-07 | PXD011960 | Pride