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Prof. Dr. Georg Häcker
Claudia Alber
Martin Büchsel
Stephanie Dille
Manuel Dold
Ian Gentle
Susanne Kirschnek
Collins Kontchou
Sophie Krüger
Arlena Metz
Isabel Mölter
Michaela Ohmer
Aparna Shenoy
Prafull Singh
Tina Tzivelekidis
Juliane Vier
Larisa Volceanov
Arnim Weber
Tom Zortel


Infections by Chlamydia trachomatis
Chlamydia trachomatis is the most frequent agent of bacterial sexually transmitted disease; its main pathogenic importance lies with pelvic inflammatory disease and infertility in female patients. There are two main aspects of chlamydial infection that we need to understand better. First, how does Chlamydia manage to live inside a human cell, to grow under the radar of the cell’s anti-bacterial defences and to be supplied with nutrients? Secondly, what are the mechanisms that lead from the infection of epithelial cells, over the recognition by immune cells, to the inflammatory damage that causes oviduct pathology and infertility? We work on both these aspects, partly in cell culture, partly in a mouse model of infection.

Neutrophil development and function
Neutrophil granulocytes are the main initial defence against bacterial infection and have substantial immunomodulatory roles in many situations. Neutrophil development can be disturbed, leading to neutropenia, and cells in the neutrophil lineage can become malignant, leading to leukaemia. We are working with a mouse model of neutrophils that we can modify genetically and study factors that determine neutrophil development and function. In some cases we also look at more complex infection models where neutrophils play important roles.

Cell death in host defence
Cell death (most often apoptosis but also other forms such as necroptosis) is one basic response that a cell has when facing challenges such as infection. Cell death plays major roles in the defence against viruses and bacteria. We have a focus on the study of molecular signalling that initiates and implements cell death. Models include cell death during chlamydial infection, during viral infection, and triggered by specific receptor signals. Molecularly, we are defining events at mitochondria and through death receptors.


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