Heat-inactivated C. pneumoniae organisms are not atherogenic.
We have previously shown that infection with Chlamydia pneumoniae can significantly exacerbate atherosclerotic lesions in LDLR-/- mice concurrently fed a high cholesterol diet in 6 or 9 months. We now report that a period of 4 month was sufficient for demonstrating the C. pneumoniae atherogenicity. However, heat inactivation of C. pneumoniae organisms completely abolished the ability of C. pneumoniae to exacerbate the atherosclerotic lesions, suggesting that viable organism infection may be required for the C. pneumoniae atherogenicity.
Sharma
Jyotika
J
Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Niu
Yuhong
Y
Ge
Jianbo
J
Pierce
Grant N
GN
Zhong
Guangming
G
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology*; D023521:Chlamydophila Infections / Q000150:complications* / Q000382:microbiology; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity*; D006358:Hot Temperature; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D011973:Receptors, LDL / Q000172:deficiency / Q000235:genetics; D013997:Time Factors
D011973:Receptors, LDL