Modulation of host cell activation and apoptosis by Chlamydia trachomatis
Chlamydiae are obligate intracellular bacteria causing respiratory (Chlamydophila pneumoniae) and urogenital infections (Chlamydia trachomatis) in man. Chlamydial infection of host cells results in resistance of infected cells to apoptosis, modulation of the expression of antigen presenting molecules (e.g. HLA class I and II), activation of anti-chlamydial factors (type I interferon system, indoleamine 2,3-dioxygenase) and expression of chemokines, cytokines and matrix metalloproteinases (MMP). During the replication cycle Chlamydiae secrete proteins into the host cell cytosol. However, there is only little knowledge on the role of these potential virulence factors in the modulation of the host cell response upon infection.
Publications
(2012) Persistent Chlamydia trachomatis infection of HeLa cells mediates apoptosis resistance through a Chlamydia protease-like activity factor-independent mechanism and induces high mobility group box 1 release. Infect Immun 80(1), 195-205. Details PubMed
(2010) Role of high-mobility group box 1 protein and poly(ADP-ribose) polymerase 1 degradation in Chlamydia trachomatis-induced cytopathicity. Infect Immun 78(7), 3288-3297. Details PubMed
Supervisor
Start of PhD
August 1, 2006
Doctoral Disputation
January 1, 2010
