De novo induction of atherosclerosis by Chlamydia pneumoniae in a rabbit model

Citation
Iw. Fong et al., De novo induction of atherosclerosis by Chlamydia pneumoniae in a rabbit model, INFEC IMMUN, 67(11), 1999, pp. 6048-6055
Citations number
45
Categorie Soggetti
Immunology
Journal title
INFECTION AND IMMUNITY
ISSN journal
00199567 → ACNP
Volume
67
Issue
11
Year of publication
1999
Pages
6048 - 6055
Database
ISI
SICI code
0019-9567(199911)67:11<6048:DNIOAB>2.0.ZU;2-Z
Abstract
Chlamydia pneumoniae, a bacterial respiratory tract pathogen, has been asso ciated with atherosclerosis in humans. C. pneumoniae infection of the respi ratory tracts of rabbits fed a noncholesterol diet induced changes of ather osclerosis of the aorta in 6 (26.1%) of 23 animals after a single inoculum at 3 months. Multiple inocula given three times within 6 weeks resulted in grade III atherosclerosis in 8 (34.8%) of 23 rabbits, with an additional 5 (21.7%) showing increased myxoid changes in the intima-media junction and e xhibiting 8 (34.8%) focal periaortitis, Control animals inoculated with car rier broth (n = 24), HEp-2 cells (n = 12), or another respiratory pathogen, Mycoplasma pneumoniae (n = 32), produced no changes of atherosclerosis aft er 3 months, The histological changes were dissimilar (fewer foam cells) fr om those of rabbits fed a 0.5% cholesterol diet but were highly similar to or indistinguishable from changes in rabbits fed a 0.15% cholesterol diet ( similar to that of humans). Proinflammatory cytokines and tissue growth fac tors were more consistently detected in cholesterol-induced aortic lesions than those induced by C. pneumoniae. These data are compatible with de novo induction of atherogenesis by C. pneumoniae in rabbits and suggest that C. pneumoniae may be important in the pathogenesis of atherosclerosis in huma ns.