Endothelial cells are protected against phagocyte-transmitted Chlamydophila pneumoniae infections by laminar shear stress: Gueinzius: Shear stress protects from C. pneumoniae infection

The respiratory pathogen Chlamydophila pneumoniae can be detected in atherosclerotic vessels, but the mechanism of dissemination from lung to vasculature remains unknown. Disturbance of vascular shear stress is a risk factor for atherosclerosis. We investigated whether polymorphonuclear neutrophils (PMN) might serve as carriers, transmitting C. pneumoniae to endothelial cells and how this is affected by shear stress. PMN were prepared from blood and incubated with C. pneumoniae. Real-time PCR and Pathfinder staining showed that after 1 h, 20% of C. pneumoniae were ingested and started to form inclusions. When infected PMN were co-incubated with HUVEC for 96 h, 10% of PMN-ingested C. pneumoniae were transmitted to HUVEC as shown by PCR and confocal microscopy. Infection of HEp-2 cells with C. pneumoniae harvested from HUVEC resulted in C. pneumoniae replication and confirmed that the bacteria remained infective. Exposure to laminar shear stress in a rotating cone-and-plate apparatus did not affect the transmission of C. pneumoniae from PMN to HUVEC, but led to a 75% reduction of inclusion formation. This can explain the focal distribution of C. pneumoniae in the vasculature and links two risk factors of atherosclerosis, i.e. the lack of laminar flow and infection.