title: Chlamydia pneumoniae infections augment atherosclerotic lesion formation: a role for serum amyloid P.
abstract: Multiple reports have demonstrated an association between Chlamydia pneumoniae (Cpn) and cardiovascular disease. In this study we evaluated the effect of Cpn infections on early lesion progression in C57BL/6J mice. Since plaque formation in these mice does not develop past the initial stage, we thought these mice might be a better model for unravelling the effect of Cpn infection on early lesion type progression. C57BL/6J mice were fed an atherogenic diet and injected 10 times with 5 x 10(7) IFU Cpn or mock. At sacrifice, lesion number, size and type were analysed. To study the role of Cpn in inflammation, serum amyloid P (SAP) in plasma was determined as well as T-cells, macrophages and SAP in the lesions. In the aortic sinus of both groups, type 2 lesions were found. Cpn infection resulted in a 2.2-fold increase in total lesion size (Cpn: 10821+/-2429 microm(2)vs mock: 5022+/-1348 microm(2); p=0.04). No difference in lesion number was observed. Also, Cpn infection increased SAP in the lesions from 1.10(-4)+/-0.1.10(-4) SAP-positive cells/lesion area to 10.10(-4)+/-1.10(-4) SAP-positive cells/lesion area (p=0.05). The influx of T-lymphocytes and macrophages in the lesions as well as SAP plasma levels were not different between groups. Multiple Cpn infections resulted in a significant increase in total lesion size of C57BL/6J mice. Increase in total SAP-positive area in infected mice suggests a role for this acute-phase protein in lesion enlargement.
authors.affiliation: Department of Surgery, University Hospital Maastricht, The Netherlands.
authors.forename: R
authors.initials: R
authors.lastname: Ezzahiri
authors.forename: F R M
authors.initials: FR
authors.lastname: Stassen
authors.forename: H R M
authors.initials: HR
authors.lastname: Kurvers
authors.forename: V
authors.initials: V
authors.lastname: Dolmans
authors.forename: P J E H M
authors.initials: PJ
authors.lastname: Kitslaar
authors.forename: C A
authors.initials: CA
authors.lastname: Bruggeman
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000097:blood / Q000382:microbiology* / Q000473:pathology; D023521:Chlamydophila Infections / Q000097:blood / Q000150:complications* / Q000382:microbiology / Q000473:pathology; D016993:Chlamydophila pneumoniae / Q000254:growth & development*; D002784:Cholesterol / Q000097:blood; D004269:DNA, Bacterial / Q000737:chemistry / Q000235:genetics; D006651:Histocytochemistry; D008264:Macrophages / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016133:Polymerase Chain Reaction; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D012850:Sinus of Valsalva / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D013047:Specific Pathogen-Free Organisms; D013601:T-Lymphocytes / Q000473:pathology; D014280:Triglycerides / Q000097:blood
chemical_list: D004269:DNA, Bacterial; D000683:Serum Amyloid P-Component; D014280:Triglycerides; D002784:Cholesterol