My research focuses on cell-autonomous immunity and bacterial evasion strategies
The introduction of antibiotics has been one of the greatest achievements in medicine. However, as bacteria develop antibiotic resistance with a tremendously fast pace, the threat has returned and there is an urgent need for finding novel ways of fighting infectious diseases.
Many pathogens have the capacity to invade human cells and to exploit the interior of their host cell as a growth niche. While human cells can sense invading microbes and can activate powerful defense programs (cell-autonomous immunity) to destroy the microbe or limit its growth, successful pathogens evolved to counteract these defenses. In my research group, we believe that a profound understanding of the molecular basis of this arms race could pave the way for innovative antimicrobials. We therefore apply state-of-the-art tools in molecular genetics and microscopic imaging, as well as high-throughput genetic and compound screening approaches, to uncover the hidden protective potential of pathogen-suppressed cellular defense programs, to identify the molecular determinants of host defense and pathogenic countermeasures, and to find means to disturb their balance to the benefit of the host.
Our current research focuses primarily on the bacterial pathogen Chlamydia trachomatis. With over 100 million cases annually, C. trachomatis is the most frequent bacterial agent of sexually transmitted diseases, and as such a common cause of infertility and adverse pregnancy outcomes. Furthermore, C. trachomatis is responsible for the ocular disease trachoma, a significant cause of visual impairment and blindness in underprivileged areas of the world. Because C. trachomatis can only grow in the interior of a human host cell, this pathogen is an exquisite model system to study cell-autonomous immunity and bacterial evasion strategies.