Changes in the adherens junctions of human endothelial cells infected with spotted fever group rickettsiae

Abstract

Rickettsiae of the spotted fever group are obligately intracellular bacteria that primarily infect the vascular endothelium, invade adjacent cells propelled by actin polymerization, and cause severe systemic diseases. Endothelial dysfunction and vascular leakage develop as a consequence; this effect is the pathophysiological mechanism that explains most clinical manifestations. Here we report that rickettsial infection of cultured primary human endothelial cells is associated with the formation of gaps in the interendothelial adherens junctions, occurring late during the course of in vitro infections but not early, even when rickettsial loads are significant.