We study molecular mechanisms of the interaction and cross-talk between pathogenic bacteria and human target cells. Pathogenic bacteria use intricate strategies to exploit the host environment, such as induction of signal transduction pathways upon attachment to host epithelial cells, extensive antigenic variation of surface components, and interaction with regulators of complement activation.

Our research focuses on bacterial pathogenesis and modulation of host cell responses by Neisseria meningitidis, Neisseria gonorrhoeae, Helicobacter pylori and Streptococcus pyogenes. How do bacteria manipulate the host defence mechanisms to survive within the host and cause disease? Understanding bacterial pathogenesis is important and will open up alternative ways to prevent, treat and cure severe infections.

The first step in the process of establishing mucosal infection is adherence of the bacteria to target cells. These processes must involve complex interactions between adhesins and corresponding receptors in each membrane. Initially the bacteria must communicate with the host, and then exploit existing signal transduction networks to intimately attach and enter into the target cell. Bacterial modulation of host cells during long-term infections can lead cell damages and cancer.

The main goal is to better understand bacterial adherence, cell signalling, invasion, and immunity. We aim to dissect critical steps of bacteria-host cell interactions, and thereby contribute to development of novel appropriate therapies and vaccines against bacterial diseases.