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

Citation
J. Tambiah et al., Provocation of experimental aortic inflammation and dilatation by inflammatory mediators and Chlamydia pneumoniae, BR J SURG, 88(7), 2001, pp. 935-940
Citations number
20
Categorie Soggetti
Surgery,"Medical Research Diagnosis & Treatment
Journal title
BRITISH JOURNAL OF SURGERY
ISSN journal
00071323 → ACNP
Volume
88
Issue
7
Year of publication
2001
Pages
935 - 940
Database
ISI
SICI code
0007-1323(200107)88:7<935:POEAIA>2.0.ZU;2-B
Abstract
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.