We are investigating which strategies Mycobacterium tuberculosis applies to cause acute and chronic infection in humans and how these strategies can be counteracted by the activity of immune cells.
The target cell that is infected by Mycobacterium tuberculosis is the human macrophage, a cell type that normally kills invading pathogens, and inside these cells the pathogen manipulates the defense functions of the cell to secure a niche for replication.
We are now taking an omics approach and use bioinformatics and systems biology to better understand how immune cells can improve their anti-mycobacterial functions. Besides clinical investigations, we also have developed advanced models to
i) study interaction of Mycobacterium tuberculosis and the human macrophage
ii), screen compound libraries to identify not only novel antibiotic compounds but also immunomodulators that enhance macrophage function and virulence blockers that prevent the bacterium from causing damage and
iii) investigate how Mycobacterium tuberculosis forms granuloma and interacts with macrophages and other cell types in tissues.
We expect our research to move the field forwards for better prevention and treatment of tuberculosis.
