title: Heat-inactivated C. pneumoniae organisms are not atherogenic.
abstract: 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.
authors.affiliation: Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
authors.forename: Jyotika
authors.initials: J
authors.lastname: Sharma
authors.forename: Yuhong
authors.initials: Y
authors.lastname: Niu
authors.forename: Jianbo
authors.initials: J
authors.lastname: Ge
authors.forename: Grant N
authors.initials: GN
authors.lastname: Pierce
authors.forename: Guangming
authors.initials: G
authors.lastname: Zhong
mesh_terms: 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
chemical_list: D011973:Receptors, LDL