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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE54336 | GEO | 2014/04/09

SECONDARY ACCESSION(S): PRJNA236228

REPOSITORIES: GEO

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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.

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

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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.

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Project description:Trachoma, a preventable blinding eye disease, is initiated by ocular infection with Chlamydia trachomatis (Ct). MicroRNA (miR) are post-transcriptional regulators of gene expression and play a major role in health and disease. We have investigated the miR profile during C. trachomatis infection of epithelial cells in vitro and in vivo during follicular trachoma with current C. trachomatis infection. Small RNA sequencing was carried out on human epithelial cells infected in vitro and on samples from five children with follicular trachoma with current Ct infection and five children with no evidence of clinical trachoma or infection. In vitro two strains of ocular Ct that differ in virulence, A2497 and isogenic plasmid-free A2497 were used to infect epithelial cell lines. RNAseq results were confirmed by qPCR in six in vitro biological replicates and in 163 clinical samples. Differential miR expression was not detected in isolated epithelial cells infected in vitro at 48 hours post infection. HCjE cells, a conjunctival epithelial cell line, have markedly different miR background expression compared to Hep2 cells. The differing miR profiles of Hep2c and HCjE suggest caution should be used when extrapolating data from Hep2 cells to a tissue-specific clinical scenario. In follicular trachoma, miR-155, miR-150, miR-142, miR-181b, miR-181a, miR-342 and miR-132 were up-regulated during current Ct infection. MiR-4728 and miR-184 were down-regulated in follicular trachoma independent of Ct infection. In follicular trachoma, miR expression reflects development and regulation of the immune response during current Ct infection and a prolonged period of wound healing following Ct clearance.

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