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ABSTRACT: Laboratory surveillance of Chlamydia trachomatis

PROVIDER: PRJEB32243 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR3288030_1.fastq.gz	Fastqsanger.gz
	ERR3288030_2.fastq.gz	Fastqsanger.gz
	ERR3288031_1.fastq.gz	Fastqsanger.gz
	ERR3288031_2.fastq.gz	Fastqsanger.gz

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Chlamydia trachomatis

Project description:Laboratory adaptation of Chlamydia trachomatis

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Progesterone activates multiple innate immune pathways in Chlamydia trachomatis-infected endocervical cells

Project description:In this project we examined the in-vitro effect of female sex hormones (estradiol and progesterone at average physiological concentrations) during a infection mediated by Chlamydia trachomatis serovar D, on the gene expression of human endometrial cell line ECC-1 The effects of the female sex hormones progesterone and oestradiol while infected by Chlamydia trachomatis were examined at two timepoints.

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Integrated phosphoproteome and transcriptome analysis reveals Chlamydia-induced epithelial-to-mesenchymal transition in host cells

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.

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Heat shock-induced transcriptomic response in Chlamydia trachomatis

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

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Project description:Human A2EN endocervical epithelial cells infected with Chlamydia trachomatis

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Indoleamine 2,3-dioxygenase cannot inhibit Chlamydia trachomatis growth in HL-60 human neutrophil granulocytes

Project description:Neutrophil granulocytes are the major cells involved in the Chlamydia trachomatis (C.trachomatis)-mediated inflammation and histopathology. A key gene in human intracellular antichlamydial defense is the tryptophan degrading enzyme indoleamine 2,3-dioxygenase (IDO), which limits the growth of the tryptophan auxotroph Chlamydia. Despite its importance, the role of IDO in the intracellular defense against Chlamydia in neutrophils has not yet been characterized. Affymetrix microarrays were used to obtain global gene expression data for monitoring the effect of C. trachomatis serovar D infection on the transcriptome of human neutrophil granulocytes.

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A GrgA-Euo-HrcA transcriptional regulatory network controls the growth and development of the obligate intracellular bacterium Chlamydia

Project description:Effects of overexpression of Chlamydia trachomatis transcription factors GrgA, Euo and HrcA on the chlamydial transcriptome were determined.

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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.

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Transcriptional profiling of human epithelial cells infected with trachoma isolates of Chlamydia trachomatis

Project description:Hep-2C cells were infected with A/2497 or B/Tunis-864 strains of Chlamydia trachomatis to compare changes in host gene expression

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