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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

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.

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Global phosphoproteome and transcriptome integration of Chlamydia trachomatis infection

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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

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

2014-04-09 | GSE54336 | GEO

Heat shock-induced transcriptomic response in Chlamydia trachomatis

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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

A primary Chlamydia trachomatis genital infection of Rhesus macaques identifies new immunodominant B-cell antigens

Project description:To identify immunodominant antigens that elicit a humoral immune response following a primary genital infection, rhesus monkeys were inoculated cervically with Chlamydia trachomatis serovar D. Serum samples were collected and probed with a protein microarray expressing 864/894 (96.4%) of the open reading frames of the C. trachomatis serovar D genome. The antibody response was analyzed in 72 serum samples from 12 inoculated monkeys. The following criteria were utilized to identify immunodominant antigens: proteins found to be recognized by at least 75% (9/12) of the infected monkeys with at least 15% elevations in normalized signal intensity from week 0 to week 8 post infection. All infected monkeys developed Chlamydia specific serum antibodies. Eight proteins satisfied the selection criteria for immunodominant antigens: CT242 (OmpH-like protein), CT541 (mip), CT681 (ompA), CT381 (artJ), CT443 (omcB), CT119 (incA), CT486 (fliY), and CT110 (groEL). Of these, three antigens, CT119, CT486 and CT381, were not previously identified as immunodominant antigens using non-human primate sera. In conclusion, these immunodominant antigens can now be tested for their ability to identify individuals with a primary C. trachomatis genital infection and to design a vaccine strategy to protect against a primary infection with this pathogen.

2020-05-27 | GSE151183 | GEO

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