|Public on Nov 21, 2011
|Chlamydia trachomatis serogroup D disturbs epithelial tissue homeostasis in Fallopian tubes via paracrine Wnt signalling
|Expression profiling by array
|Chlamydia trachomatis is the causative agent of sexually transmitted disease with the highest prevalence in the world today. Although, sensitive to antibiotic treatment, Ctr is also a major cause of infertility due to significant cell damage caused to the genital tract of affected women. Occlusion of Fallopian tubes is a frequent consequence of advanced ascending Ctr infection. So far the mechanisms of Ctr caused pathogensis are widely unclear. Here we show, by using an ex vivo infection model of human Fallopian tubes that Ctr causes changes in epithelial homeostasis within 2 days of inoculation, by disrupting cell adhesion and increasing cell proliferation. We demonstrate by imaging and expression analysis that tissue response to invading pathogen has also a paracrine component. We identify Wnt signalling activation as one of the hallmarks of Ctr infection which transmits effects of the infection beyond inclusion containing cells. Mechanisms of phenotypic changes involve up regulation of Epcam and Olfactomedin 4, biomarkers and regulators of cell adhesion and cell differentiation. Our findings bring focus to the pleiotropic effects of Ctr infection within epithelium and could be provide the basis for better understanding the pathological sequels in vivo.
|Microarray experiments were performed as dual-color hybridizations. To compensate for dye-specific effects, an independent dye-reversal color-swap was applied. Quality control and quantification of total RNA amount was assessed using an Agilent 2100 bioanalyzer (Agilent Technologies) and a NanoDrop 1000 spectrophotometer (Kisker).
|Kessler M, Meyer TF, Fotopoulou C, Mollenkopf H
|Jan 19, 2011
|Last update date
|Feb 22, 2018
|+49 30 28460 482
|Max-Planck-Institute for Infection Biology
|Microarray/Genomics Core Facility
|Agilent-014850 Whole Human Genome Microarray 4x44K G4112F (Feature Number version)