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Human enteroendcrine cell responses to infection with Chlamydia trachomatis

ABSTRACT: The aim of this study was to perform a microarray analysis of the response pattern of EEC from both large and small bowel to infection in vitro, using Chlamydia trachomatis infection as a model.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58151 | GEO | 2014/06/03

SECONDARY ACCESSION(S): PRJNA251395

REPOSITORIES: GEO

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Human enteroendcrine cell responses to infection with Chlamydia trachomatis

Project description:The aim of this study was to perform a microarray analysis of the response pattern of EEC from both large and small bowel to infection in vitro, using Chlamydia trachomatis infection as a model. Two human EEC lines: LCC-18, derived from a neuroendocrine colonic tumour, and CNDT-2, derived from a small intestinal carcinoid, were infected with C. trachomatis serovar LGV II strain 434 (ATCC VR-902B). Penicillin G was used to induce persistent infection. Gene expression levels in infected and persistently infected EEC cells were investigated by microarray analysis

2014-06-03 | E-GEOD-58151 | biostudies-arrayexpress

Global phosphoproteome and transcriptome integration of Chlamydia trachomatis infection

Project description:Gene expression profiles of RNA extracted at 24 or 48h from End1 cells infected with Chlamydia trachomatis or uninfected controls. This experiment forms part of the analysis of phosphoproteome changes after C.trachomatis infection.

2019-01-16 | GSE104166 | GEO

Transcriptome profiling of endometrial biopsies inflammatory response to Chlamydia trachomatis genital tract infection

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

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

Transcriptome profiling of endometrial biopsies inflammatory response to Chlamydia trachomatis genital tract infection

2013-03-01 | GSE41075 | GEO

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.

2011-08-02 | E-GEOD-31149 | biostudies-arrayexpress

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

2014-04-09 | GSE54336 | GEO

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

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 effector Dre1 interacts with dynactin to reposition host organelles during infection.

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

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