Molecular pathogenesis of chronic Chlamydia pneumoniae infection: a brief overview

Abstract

Owing to its unique host cell-dependent development cycle, Chlamydia pneumoniae occupies an intracellular niche that enables the bacterium to survive and to multiply, secluded from both the extracellular and the cytoplasmic environments. Within its separate chlamydial inclusion, it is able to genetically switch between a replicative and a persisting non-replicative state, linking the pathogen to acute as well as chronic diseases. Although its role in acute respiratory infection has been established, a potential link between chronic vascular infection with C. pneumoniae and the development of atherosclerosis remains enigmatic, in particular because chronic chlamydial infection cannot be eradicated by antibiotics. C. pneumoniae has developed numerous mechanisms to establish an adequate growth milieu involving the type III secretion-mediated release of chlamydial effector proteins that interact with cellular structures and reprogram host cell regulatory pathways. This brief overview of these pathomechanisms focuses on chronic vascular infection.