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
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.