TITLE:
Involvement of TLR2 and TLR4, Chlamydophila pneumoniae and Mycoplasma pneumoniae in adventitial inflammation of aortic atherosclerotic aneurysm
AUTHORS:
Renata Melo de Assis, Maria de Lourdes Higuchi, Marcia Martins Reis, Suely A. P. Palomino, Rosario Dominguez Crespo Hirata, Mario Hiroyuki Hirata
KEYWORDS:
Aortic Atherosclerotic Aneurysm; Inflammation; Co-Infection; Chlamydophila pneumoniae; Mycoplasma pneumoniae; Toll-Like Receptors
JOURNAL NAME:
World Journal of Cardiovascular Diseases,
Vol.4 No.1,
January
17,
2014
ABSTRACT: Aortic atherosclerotic aneurysm (AAA) is associated
with adventitial inflammation where infection is suggested to have a role.
Co-infection with Chlamydophila pneumoniae (Cp) and Mycoplasma
pneumoniae (Mp) was linked with coronary plaque rupture, in association
with vessel dilatation and adventitial inflammation. Pathogens are recognized
by Toll-like receptors (TLRs) development of the inflammatory process. Objective:
Here, we studied whether co-infection by Cp and Mp was involved in the increased
inflammation present in AAA and if it could be associated with deficient
expression of TLRs. We compared human samples of AAA with non-dilated human aortic
atherosclerotic lesions, regarding the amount of Cp and Mp antigens, and
expression of TLR2 and TLR4. Methods: Two groups of aorta fragments were
analyzed: G1 (n = 13) moderate atherosclerosis and G2 (n = 14) AAA samples,
through immunohisto-chemistry and in situ hybridization methods. Results: Mp and Cp antigens in intima/medial
layer were greater in G2 than G1, with no difference in adventitia. TLR2 and
TLR4 were higher in G2 than G1 adventitia fat. There was a correlation between
Mp versus TLR2 and of TLR4 in intima/medial layer and in adventitia of G1, but
there was a lack of correlation in G2. In Cp adventitia, the correlation in G1
was high with TLR2 but not with TLR4, and in G2 the correlation was positive
for both TLRs. Conclusion: This study favors the concept that symbiotic
co-infection by Cp and Mp participates in the pathogenesis of AAA. It also
emphasizes that adventitial fat is the initial site for colonization of these
bacteria that probably reach the tissue through vasa vasorum. An exacerbated immune reaction is not efficient to
control the infection that reaches and proliferates in high levels at the
medial and intimal layer, contributing to the development of vessel dilatation.