Role of Chlamydia pneumoniae in an experimental animal model of aneurysm formation

Background: Chlamydia pneumoniae has been implicated in the pathogenesis of vascular disease. C. pneumoniae DNA is present in 40–50 per cent of abdominal aortic aneurysm biopsies. This study investigated whether C. pneumoniae has a causal role in experimental aortic dilatation. Methods: Experimental aneurysms were established in cholesterol‐fed rabbits by periaortic application of calcium chloride solution and a combination of thioglycollate (a non‐specific macrophage activator) or C. pneumoniae (live, formalin fixed or heat inactivated at 10 8 organisms per ml). After 3 weeks, aortic diameter was measured and aortas were harvested for analysis of macrophage counts. C. pneumoniae DNA was measured by polymerase chain reaction and C. pneumoniae antigens (both membrane and heat shock protein 60) were determined by immunostaining. Results: Live or formalin‐fixed C. pneumoniae at concentrations of 10 8 organisms per ml mimicked the effects of thioglycollate to produce aortic dilatation associated with macrophage influx. Lower concentrations of C. pneumoniae had a minimal effect.Substance applied to aorta Increase in aortic diameter (%) C. pneumoniae DNA positive C. pneumoniae antigen positive Macrophage count per unit areaCalcium chloride only (control) 19(7) 0 of 6 — 5·61(6·4) Thioglycollate 112(19) * 0 of 8 — 29·6(45) *C. pneumoniaeLive 125(25) * 2 of 4 Yes 342(144) *Formalin fixed 98(198) * 2 of 5 Yes 143(69) * Heat inactivated 54(16) * 0 of 4 No 26·6(15) ** P < 0·05 versus control (analysis of variance)Conclusion: In this experimental study, high doses of C. pneumoniae membrane antigens stimulated macrophage influx and aortic dilatation. Lipopolysaccharide had a lesser effect. C. pneumoniae antigens could contribute to an in vivo aggregate pathogen burden by provoking an inflammatory response. © 2001 British Journal of Surgery Society Ltd