title: Respiratory infection in lipid-fed rabbits enhances sudanophilia and the expression of VCAM-1.
abstract: The pathogenesis of atherosclerosis has been related to infection of the arterial wall, but it is not clear whether this occurs before or after the development of lipid-containing lesions. Respiratory bacterial infection increases the expression of vascular cell adhesion molecule-1 (VCAM-1). We therefore examined whether a similar infection would enhance atherosclerosis in New Zealand White rabbits fed chow supplemented by 15% (w/w) egg yolk for 50 days. Rabbits with naturally acquired respiratory infection by Pasteurella multocida, pathogen-free (SPF) animals infected by P. multocida in the laboratory, and age-matched SPF rabbits maintained in a disease-free environment were used. Endothelial cells expressing VCAM-1 in the aorta between intercostal arteries 3 and 5 were identified using anti-VCAM-1 (Rb1/9) and an alkaline-phosphatase-linked secondary antibody and quantified in Häutchen preparations. The remainder of the aorta was stained with Sudan IV to show lipid deposition. The expression of VCAM-1 (mean +/- SEM per 10,000 cells) was 22 +/- 8 (n = 5) in the lipid-fed SPF rabbits, significantly different from that in the lipid-fed rabbits with naturally occurring infection (190 +/- 51 (n = 5)) or from rabbits infected in the laboratory (106 +/- 25 (n = 5)). The extent of Sudanophilia was significantly greater in the naturally infected rabbits (8.3 +/- 1.2%) or infected SPF rabbits (10.3 +/- 1.8%) than in the SPF rabbits (2.7 +/- 0.8%; P < 0.05). Antibiotic treatment in naturally infected rabbits reduced the number of cells expressing VCAM-1 and the extent of the Sudanophilia to baseline levels. Thus, Sudanophilia is enhanced by bacterial infection in rabbits fed egg yolk and is associated with a significant increase in VCAM-1.
authors.affiliation: Department of Pathology, McMaster University, Hamilton, Ontario, Canada.
authors.forename: M
authors.initials: M
authors.lastname: Richardson
authors.forename: M
authors.initials: M
authors.lastname: De Reske
authors.forename: K
authors.initials: K
authors.lastname: Delaney
authors.forename: A
authors.initials: A
authors.lastname: Fletch
authors.forename: L H
authors.initials: LH
authors.lastname: Wilcox
authors.forename: R L
authors.initials: RL
authors.lastname: Kinlough-Rathbone
mesh_terms: D000818:Animals; D000890:Anti-Infective Agents / Q000494:pharmacology; D001013:Aorta, Thoracic / Q000378:metabolism / Q000648:ultrastructure; D001161:Arteriosclerosis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D001391:Azo Compounds; D002452:Cell Count; D002784:Cholesterol / Q000097:blood; D004396:Coloring Agents; D004041:Dietary Fats / Q000009:adverse effects*; D004730:Endothelium, Vascular / Q000378:metabolism; D000077422:Enrofloxacin; D024841:Fluoroquinolones; D010326:Pasteurella Infections / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D016979:Pasteurella multocida / Q000472:pathogenicity; D018410:Pneumonia, Bacterial / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D015363:Quinolones / Q000494:pharmacology; D011817:Rabbits; D013047:Specific Pathogen-Free Organisms; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis* / Q000276:immunology
chemical_list: D000890:Anti-Infective Agents; D001391:Azo Compounds; D004396:Coloring Agents; D004041:Dietary Fats; D024841:Fluoroquinolones; D015363:Quinolones; D019010:Vascular Cell Adhesion Molecule-1; D000077422:Enrofloxacin; D002784:Cholesterol; C009213:Scarlet Red