Endothelial Dysfunction After Repeated<i>Chlamydia pneumoniae</i>Infection in Apolipoprotein E–Knockout Mice

Abstract

C pneumoniae impairs arterial endothelial function, and the NO pathway is principally involved. Cyclooxygenase-dependent vasoconstricting products may also account for the infection-induced impaired relaxation. These findings further support the role of C pneumoniae infection in atherosclerosis development.