Wassef, M., Baxter, B.T., Chisholm, R.L., Dalman, R.L., Fillinger, M.F., Heinecke, J., Humphrey, J.D., Kuivaniemi, H., Parks, W.C., Pearce, W.H., Platsoucas, C.D., Sukhova, G.K., Thompson, R.W., Tilson, M.D. and Zarins, C.K. (2001) Pathogenesis of abdominal aortic aneurysms: A multidisciplinary research program supported by the National Heart, Lung, and Blood Institute. Journal of Vascular Surgery, 34, 730738
http://dx.doi.org/10.1067/mva.2001.116966

has been cited by the following article:

• 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.