Chlamydia pneumoniae and Mycoplasma pneumoniae can induce inflammatory process in AMI: proposal mechanisms by CD14 and TLRs.

Abstract

Evidences has been shown that receptors CD14 and TLR are involved in the mechanism of microorganism components recognition responsible for the initiation of inflammatory response inducing the expression of IL-6 and TNF-alpha which can be responsible for the beginning process of endothelial lesion or the instabilization of the atheroma plaque. Polymorphism in the CD14, TLRs and cytokines genes can changes its expressions and modify the protein sequence consequently in the inflammatory response and exacerbating or reducing susceptibility to infections. The aims of this study will be a case control study to evaluate the participation of the inflammatory response induced by infectious agents through the membrane receptors (CD14 and TLRs) and pro-inflammatory proteins (IL-6 and TNF-alpha) in patients with acute myocardial infarction (AMI). Also evaluate the possible association between polymorphisms of genes CD14, TLR2, TLR4, IL-6 and TNF-alpha and its activity, as well as their relationship with the IAM. Real-time PCR will be used to quantity Chlamydia pneumoniae and Mycoplasma Pneumoniae, to genotype and quantitify the expression of genes CD14, TLR2, TLR4, IL-6 and TNF-alpha using GAPD gene as control of reaction. Immunochemistry methods will be used to evaluate the IgG and IgA plasma anti-C. pneumoniae and anti-M. pneumonia and determine concentrations of Interleukin-6 and TNF-alpha. The results of this research will give important information to clarifying the involvement of infectious agents and their relationship with acute myocardial infarction.