Chronic perivascular inoculation with Chlamydophila pneumoniae results in plaque formation in vivo
| Autor: | Markus G. Engelmann, Sigrid Nikol, Jaroslav Pelisek, Constanze Veronika Redl, Corinna Barz, Juergen Heesemann |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Lipopolysaccharides
Pathology medicine.medical_specialty Lipopolysaccharide Normal diet medicine.medical_treatment Hypercholesterolemia Sodium Chloride Biology medicine.disease_cause Pathology and Forensic Medicine Cholesterol Dietary Lesion Random Allocation chemistry.chemical_compound In vivo Cell Line Tumor medicine Animals Chlamydophila Infections Molecular Biology Saline Histology Arteries Cell Biology Chlamydophila pneumoniae Atherosclerosis C-Reactive Protein medicine.anatomical_structure chemistry Connective Tissue Diet Atherogenic Female Rabbits medicine.symptom Tunica Media Blood vessel |
| Zdroj: | Laboratory Investigation. 86:467-476 |
| ISSN: | 0023-6837 |
| Popis: | Hypercholesterolemic and normocholesterolemic rabbit models of chronic arterial Chlamydophila (Chlamydia) pneumoniae (CPN) inoculation were established and the role of both viable and inactivated bacteria was investigated in atherogenesis. A total of 29 rabbits were randomized to four groups. Groups A and B were fed a cholesterol-enriched diet, and groups C and D were fed a normal diet. Arterial segments of group A and C animals were inoculated in vivo using viable CPN chronically using repeated perivascular applications. Contralateral arteries were treated using heat-inactivated CPN. Group B and D animals were treated with repeated perivascular injections of bacterial lipopolysaccharide (LPS) and saline (control). Additional hypercholesterolemic rabbits were treated by repeated injections using viable and inactivated CPN, each controlled by saline injections. To compare the effects of this chronic inoculation model, additional animals received single injections of either viable CPN, inactivated CPN, LPS, or saline. Vascular tissues (n=162 treated arteries of 29 rabbits) were analyzed using morphometry at histology. CPN was detected by fluorescence-immunohistochemistry and nested polymerase chain reaction. Only in hypercholesterolemic, but not in normocholesterolemic rabbits, chronic perivascular infection of all bacterial components, viable and heat-inactivated CPN, as well as LPS resulted in a significant increase in atheromatous lesion formation (lesion area index: 0.23+/-0.08, 0.25+/-0.09, and 0.15+/-0.05) when compared to controls (lesion area index 0.01+/-0.01, P=0.002). CPN persisted in atheromatous lesions and vascular tissues. Single perivascular infection using CPN or inactivated CPN was not able to induce lesion formation (lesion area index: 0.03+/-0.03, 0.03+/-0.02 vs 0.03+/-0.02 after single saline inoculation, P=0.965). In conclusion, chronic vascular infection with CPN or CPN components acts as a cofactor requiring other major atherogenic stimuli, rather than as a causative agent. |
| Databáze: | OpenAIRE |
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