Chlamydia pneumoniae heat shock protein 60 is associated with apoptotic signaling pathway in human atheromatous plaques of coronary artery disease patients

SummaryBackgroundChlamydia pneumoniae heat shock protein (HSP) 60 is known to contribute to the activation of inflammation. In addition, there are contradictory reports on C. pneumoniae and their role in activation of pathways (apoptotic/antiapoptotic/necrosis) in coronary artery disease (CAD). Hence, more studies are required to know the actual role of C. pneumoniae in activation of apoptotic/antiapoptotic/necrosis pathways.Methods and resultsIn this study, two sets of patient groups (cHSP60 positive and cHSP60 negative) were included and gene expression was studied by cDNA micro array and real time polymerase chain reaction arrays. Expression of Caspase-3, 8, 9, c-FLIP, PPAR-γ, PGC-1α, and Gsk-3b were also evaluated at protein level by immunoblotting. In cHSP60 positive CAD patients significantly higher (p < 0.001) mRNA expression was found for CCL4, CXCL4, CXCL9, IL-8, CD40LG, CD8, TGFβ1, TGFβ2, APOE, EGR1, CTGF, APOB, LDLR, LPA, and LPL, whereas significantly lower (p < 0.001) mRNA expression was detected for CD4, IL1F10, IFNA2, and IL-10 as compared to cHSP60 negative CAD patients. Additionally, at protein level expression of Caspase-3 (p = 0.027), 8 (p = 0.028), and 9 (p = 0.037) were higher and c-FLIP (p = 0.028) and PPAR-γ (p = 0.95) expression were comparable in cHSP60 positive CAD patients compared to cHSP60 negative CAD patients.ConclusionGenes/proteins of pre-apoptotic caspase dependent/independent pathways, chemokines, and inflammatory cytokines receptors were significantly up-regulated in human atheromatous plaques of cHSP60 positive CAD patients suggesting an association of cHSP60 with CAD.