Author’s Reply: Microorganisms and valve tissue/ Demonstration of Chlamydophila pneumoniae, Mycoplasma pneumoniae, Cytomegalovirus, and Epstein-Barr virus in atherosclerotic coronary arteries, nonrheumatic calcific aortic and rheumatic stenotic mitral valves by polymerase chain reaction

We agree with the information that authors of the letter have shared with us. We are thankful for their interest in our study (1). Additionally, we want to answer their questions about the potential role of microorganisms in the pathogenesis of atherosclerosis. The hypothesis that several bacterial and viral agents may induce the progression of atherosclerosis has been extensively studied for two decades. Several studies have suggested an association between infectious agents and atherosclerosis (2, 3). These microorganisms not only bear triggering mechanisms for ongoing inflammations, they also have proactive roles in fibrotic tissue progression. They may comprise triggering factors for the initiation and/ or acceleration of an ongoing inflammatory process by increased expression of adhesion molecules and inflammatory cytokines, procoagulant effects, increased receptor expression and activity, enhanced uptake of cholesterol and of modified low-density lipoprotein, increased smooth muscle cell migration and proliferation, anti-apoptotic effects, and autoimmune response to infection (4).