Background and current state of research
Infections with Chlamydia trachomatis are the leading cause of infectious tubal infertility worldwide. More than 89 Mio cases of sexually transmitted C. trachomatis infections are newly diagnosed per year. Chlamydiae are obligate intracellular bacteria that all share a unique biphasic developmental cycle that allows the pathogen to persist inside its host cells and cause chronic inflammatory tissue damage. We hypothesize that local changes in the microenvironment affect host immune response directed against intracellular chlamydiae and lead to chronic inflammation with severe sequelea.
Our goals
C. trachomatis infections are the most prevalent sexually transmitted infections (STI) worldwide and can lead to various diseases such as pelvic inflammatory disease (PID) and salpingitis. Furthermore, ectopic pregnancies and infertility are often caused by chronic infections with C. trachomatis. Environmental conditions such as oxygen content or availability of nutrients influence host defence functions and the metabolism of the pathogen. In our project, we aim to investigate the microbial community populating the female genital tract as a complex micro-environmental factor influencing the pathogenicity of Chlamydia trachomatis.
How to get there
To understand the influence of the microbial community within the female genital tract on the pathogenicity of C. trachomatis, we investigate bacterial community structure in a group of healthy females, a group of females prone to infections with C. trachomatis and a group of non-fertile females using next generation sequencing. Based on these results, we establishe cell culture experiments, experiments with explanted human fallopian tubes and mouse experiments to analyze the influence of identified microbial components on the pathogenicity of C. trachomatis in vitro and in vivo.
More information
Max Planck Institute for Evolutionary Biology
[1] Fluorescence lifetime imaging unravels C. trachomatis metabolism and its crosstalk with the host cell. Szaszák M, Steven P, Shima K, Orzekowsky-Schröder R, Hüttmann G, König IR, Solbach W, Rupp J. PLoS Pathog. 2011 Jul;7(7):e1002108.
[2] Hypoxia abrogates antichlamydial properties of IFN-γ in human fallopian tube cells in vitro and ex vivo. Roth A, König P, van Zandbergen G, Klinger M, Hellwig-Bürgel T, Däubener W, Bohlmann MK, Rupp J. Proc Natl Acad Sci U S A. 2010 Nov 9;107(45):19502-7.