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.
Project description:In this project we examined in-vitro effect of female sex hormones, estradiol and progesterone at average physiological concentration level on Chlamydia trachomatis gene expression level.
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
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.
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.
Project description:In this project we examined in-vitro effect of female sex hormones, estradiol and progesterone at average physiological concentration level on Chlamydia trachomatis gene expression level. Regulation of chlamydial gene expression by the female sex hormones oestradiol and progesterone was examined. A total of 16 chlamydial arrays were analysed with the 4 culture conditions (no hormone, E, P, E+P) x four replicates. Bacterial samples were grown in non-hormone treated culture were used as control
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.