Chlamydophila pneumoniae infection induces alterations in vascular contractile responses.
Chlamydophila pneumoniae infection has been associated in previous studies with coronary artery disease. The live bacterium has been detected within atherosclerotic plaques and can induce the structural remodeling of the vessel wall. However, the direct effects of infection on the contractile characteristics of the arteries remain unknown. Left anterior descending coronary arteries isolated from porcine hearts were dissected and placed in culture medium for 72 hours before infection with C. pneumoniae. Contractile responses to high molar KCl and u46619 levels and relaxation responses to bradykinin and sodium nitroprusside were assessed at days 5 and 10 postinfection. C. pneumoniae induced decreases in both KCl- and u46619-induced contractile responses at both time points. The altered contractile responses coincided with a down-regulation of L-type Ca(2+) channels at both time points and inositol 1,4,5-triphosphate receptor (IP3R) levels at day 10 postinfection. Infection also induced attenuation of the endothelial-dependent relaxation response to bradykinin at day 10 postinfection. A decrease in endothelial nitric oxide synthase expression levels was noted at day 10 postinfection. Furthermore, an increase in superoxide production combined with an increase in p22phox expression levels was also observed at this time point. These findings indicate that C. pneumoniae infection can directly alter the vascular contractile responses in porcine coronary arteries, providing additional evidence for the role of C. pneumoniae infection in cardiovascular disease.
Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Department of Physiology, Faculties of Medicine and Pharmacy, University of Manitoba, Winnipeg, Manitoba, Canada.
Justin F
JF
Deniset
Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Department of Physiology, Faculties of Medicine and Pharmacy, University of Manitoba, Winnipeg, Manitoba, Canada.
Thomas E
TE
Hedley
Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Department of Physiology, Faculties of Medicine and Pharmacy, University of Manitoba, Winnipeg, Manitoba, Canada.
Elena
E
Dibrov
Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Department of Physiology, Faculties of Medicine and Pharmacy, University of Manitoba, Winnipeg, Manitoba, Canada. Electronic address: gpierce@sbrc.ca.
Grant N
GN
Pierce
D000818:Animals; D020746:Calcium Channels, L-Type / Q000502:physiology; D018834:Chaperonin 60 / Q000378:metabolism; D023521:Chlamydophila Infections / Q000503:physiopathology*; D016993:Chlamydophila pneumoniae; D003327:Coronary Disease / Q000382:microbiology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism; D006801:Humans; D009119:Muscle Contraction / Q000502:physiology*; D009126:Muscle Relaxation / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D019255:NADPH Oxidases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D034421:Sus scrofa; D051197:Toll-Like Receptor 4 / Q000378:metabolism
D020746:Calcium Channels, L-Type; D018834:Chaperonin 60; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D013481:Superoxides; D052250:Nitric Oxide Synthase Type III; D019255:NADPH Oxidases; C086986:CYBA protein, human