title: Chlamydophila pneumoniae (Chlamydia pneumoniae) accelerates the formation of complex atherosclerotic lesions in Apo E3-Leiden mice.
abstract: OBJECTIVE
  Atherosclerosis is an inflammatory process and is characterised by the presence of T-lymphocytes in the lesions. To study the role of Chlamydophila pneumoniae (C. pneumoniae) in this process and the effect of infection on T-cell influx, we infected Apo E3-Leiden mice with C. pneumoniae and investigated the effect on lesion development and T-cell influx in atherosclerotic lesions at different time points post infection (pi).
  
  
  METHODS
  Nine week old mice, fed an atherogenic diet, were either mock-infected or infected with C. pneumoniae and sacrificed at 1, 6 and 9 months pi. Longitudinal sections of the aortic arches of the mice were stained with hematoxylin-eosin for atherosclerotic lesion type and lesion area analysis, or with rabbit-anti-CD3(+) to detect the presence of T-cells in the atherosclerotic lesions. T-cell influx was expressed as number of T-lymphocytes/lesion area.
  
  
  RESULTS
  At 1 month pi, type 1, 2 and 3 lesions were present. At other time points pi, more complex lesion types 4, 5a and 5b were also present. Although infection did not influence the total lesion number or area, we observed an effect of C. pneumoniae infection on lesion type. Infection resulted in a significant shift in lesion formation from type 3 to type 4 (P=0.022) at 6 months pi, and from type 4 to type 5a (P=0.002) at 9 months pi. T-cells were observed at every time point pi. At 1 month pi, a significant increase in T-cell influx in the C. pneumoniae-infected atherosclerotic lesions was observed (P=0.0005).
  
  
  CONCLUSIONS
  This study shows that C. pneumoniae infection enhances the inflammatory process by increasing T-lymphocytes in the plaque and accelerates the formation of complex lesions.
authors.affiliation: Department of Surgery, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 5800, 6202 AZ, Maastricht, The Netherlands. rajaa_ezzahiri@hotmail.com
authors.forename: R
authors.initials: R
authors.lastname: Ezzahiri
authors.forename: H J M G
authors.initials: HJ
authors.lastname: Nelissen-Vrancken
authors.forename: H A J M
authors.initials: HA
authors.lastname: Kurvers
authors.forename: F R M
authors.initials: FR
authors.lastname: Stassen
authors.forename: I
authors.initials: I
authors.lastname: Vliegen
authors.forename: G E L M
authors.initials: GE
authors.lastname: Grauls
authors.forename: M M L
authors.initials: MM
authors.lastname: van Pul
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; D001025:Aortitis / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D001161:Arteriosclerosis / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D002690:Chlamydia Infections / Q000150:complications*; D016993:Chlamydophila pneumoniae; D002784:Cholesterol / Q000097:blood; D004036:Diet, Atherogenic; D018450:Disease Progression; D005260:Female; D006937:Hypercholesterolemia / Q000150:complications; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D012307:Risk Factors; D013601:T-Lymphocytes / Q000473:pathology; D014280:Triglycerides / Q000097:blood
chemical_list: D014280:Triglycerides; D002784:Cholesterol