Provocation of experimental aortic inflammation and dilatation by inflammatory mediators and Chlamydia pneumoniae

Background: The macrophage appears to have a key role in the inflammation a nd proteolysis associated with the growth and development of abdominal aort ic aneurysms. The role of inflammatory mediators and Chlamydia pneumoniae i n stimulating the influx of macrophages and dilatation of the abdominal aor ta was investigated in an experimental model. Methods: Periaortic application of calcium chloride solution (and monocyte chemoattractant protein (MCP) 1, a cocktail of cytokines or C. pneumoniae) to the abdominal aorta of New Zealand White rabbits was performed at laparo tomy. Some animals were fed a cholesterol-rich diet. The diameter of the ao rta was measured by ultrasonography and after perfusion fixation, 3 weeks a fter laparotomy. Aortic sections were stained with RAM-11 to identify macro phages for counting. The presence of C. pneumoniae DNA was confirmed using the polymerase chain reaction. Results: Aortic macrophage influx in response to MCP-1, thioglycollate or C . pneumoniae was more than doubled in the cholesterol-fed animals. In respo nse to human recombinant MCP-1 (1 mug) the mean(s.d.) macrophage count incr eased from 79(19) to 340(215) per unit area (P < 0.02). Even in cholesterol -fed animals, application of MCP-1 (recombinant human or rabbit form) was n ot associated with aortic dilatation. Application of thioglycollate 0.1 mol /l, or live or formalin-inactivated C. pneumoniae (0.5 x 10(8) organisms), was associated with a similar increase in macrophages to that caused by MCP -1 and a significant (approximately twofold) increase in aortic diameter af ter 3 weeks. Conclusions: Macrophage influx into rabbit abdominal aorta, without macroph age activation, is insufficient to cause experimental aortic dilatation. C. pneumoniae antigens appeared to stimulate aortic dilatation, probably by s pecific activation of macrophages.