%0 Journal Article
%T Involvement of TLR2 and TLR4, <i>Chlamydophila  pneumoniae</i> and <i>Mycoplasma pneumoniae</i> in adventitial  inflammation of aortic atherosclerotic aneurysm
%A Renata Melo de Assis
%A Maria de Lourdes Higuchi
%A Marcia Martins Reis
%A Suely A. P. Palomino
%A Rosario Dominguez Crespo Hirata
%A Mario Hiroyuki Hirata
%J World Journal of Cardiovascular Diseases
%P 14-22
%@ 2164-5337
%D 2014
%I Scientific Research Publishing
%R 10.4236/wjcd.2014.41004
%X <p style=\"text-align:justify;\">
	<span style=\"font-size:10.0pt;\"><span style=\"font-family:Verdana;\">Aortic atherosclerotic aneurysm (AAA) is associated
with adventitial inflammation where infection is suggested to have a role.
Co-infection with </span><i><span style=\"font-family:Verdana;\">Chlamydophila pneumoniae</span></i><span style=\"font-family:Verdana;\"> (Cp) and </span><i><span style=\"font-family:Verdana;\">Mycoplasma
pneumoniae</span></i><span style=\"font-family:Verdana;\"> (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. </span><i><span style=\"font-family:Verdana;\">Objective</span></i><span style=\"font-family:Verdana;\">:
Here, we studied whether co-infection by </span><i><span style=\"font-family:Verdana;\">Cp</span></i><span style=\"font-family:Verdana;\"> and </span><i><span style=\"font-family:Verdana;\">Mp </span></i><span style=\"font-family:Verdana;\">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. </span><i><span style=\"font-family:Verdana;\">Methods:</span></i><span style=\"font-family:Verdana;\"> Two groups of aorta fragments were
analyzed: G1 (n = 13) moderate atherosclerosis and G2 (n = 14) AAA samples,
through immunohisto-chemistry and </span><i><span style=\"font-family:Verdana;\">in situ</span></i><span style=\"font-family:Verdana;\"> hybridization methods. </span><i><span style=\"font-family:Verdana;\">Results</span></i><span style=\"font-family:Verdana;\">: 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. </span><i><span style=\"font-family:Verdana;\">Conclusion</span></i><span style=\"font-family:Verdana;\">: 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
%K Aortic Atherosclerotic Aneurysm
%K Inflammation
%K Co-Infection
%K &lt
%K i&gt
%K Chlamydophila pneumoniae&lt
%K /i&gt
%K &lt
%K i&gt
%K Mycoplasma pneumoniae&lt
%K /i&gt
%K Toll-Like Receptors
%U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=42118