Complement escape mechanisms of Streptococcus pneumoniae
My project aims on complement escape strategies used by the human pathogenic bacteria Streptococcus pneumoniae. Upon infection S.pneumoniae similar to other pathogenic microbes is constantly challenged by the complement defense system of the human host. The complement system as a part of the innate immune system forms a human line of defence that recognizes and damages infectious microbes. Complement is activated by three pathways: the alternative, the classical and the lectin pathway. Pathogenic microbes have developed diverse mechanisms to evade host complement system.
Streptococcus pneumoniae is a facultative human pathogen that can cause pneumonia, acute sinusitis, otitis media, bacteraemia and meningitis. S. pneumoniae binds the human plasma protein Factor H, which is the central inhibitor of the alternative complement pathway. Factor H bound to the bacterial surface protects the pathogen from the damaging effects of the complement cascade. My project deals with identifying complement escape strategies used by S. pneumoniae. Particularly, I want to identify and characterise bacterial proteins that bind host complement inhibitors. I aim to study interactions of streptococcal surface proteins with regulators of the complement and coagulation cascades.
Start of PhD
January 1, 2011
March 19, 2014