Chlamydia pneumoniae Infection in Atherosclerotic Lesion Development through Oxidative Stress: A Brief Overview

Abstract

Chlamydia pneumoniae, an obligate intracellular pathogen, is known as a leading cause of respiratory tract infections and, in the last two decades, has been widely associated with atherosclerosis by seroepidemiological studies, and direct detection of the microorganism within atheroma. C. pneumoniae is presumed to play a role in atherosclerosis for its ability to disseminate via peripheral blood mononuclear cells, to replicate and persist within vascular cells, and for its pro-inflammatory and angiogenic effects. Once inside the vascular tissue, C. pneumoniae infection has been shown to induce the production of reactive oxygen species in all the cells involved in atherosclerotic process such as macrophages, platelets, endothelial cells, and vascular smooth muscle cells, leading to oxidative stress. The aim of this review is to summarize the data linking C. pneumoniae-induced oxidative stress to atherosclerotic lesion development.

Chlamydia Pneumoniae and Cardiovascular Disease in End-Stage Renal Disease Patients: An Update

“…In atherosclerosis, the involvement of e. pneumoniae, a respiratory pathogen, has been supported by seroepidemiology, identification of the microorganism within atheroma by immunochemistry and electron microscopy, and direct detection of chlamydial DNA within atheroma by polymerase chain reaction (PCR) (13)(14)(15). Several in vivo studies have shown that e. pneumoniae contributes to exacerbation of lesions in hyperlipidaemic animal models, suggesting thatthis microorganism is aco-risk factor with hyperlipidaemia (15).…”

“…Several in vivo studies have shown that e. pneumoniae contributes to exacerbation of lesions in hyperlipidaemic animal models, suggesting thatthis microorganism is aco-risk factor with hyperlipidaemia (15). In addition, in vitro studies have demonstrated that this microorganism is able to disseminate systematically from the lungs through infected peripheral blood mononuclear cells (PBMC) and to localize in multiple tissues, including the arterial wall (16,17).…”

“…In addition, in vitro studies have demonstrated that this microorganism is able to disseminate systematically from the lungs through infected peripheral blood mononuclear cells (PBMC) and to localize in multiple tissues, including the arterial wall (16,17). As a result, e. pneumoniae may infect monocytes/macrophages, endothelial cells and vascular smooth muscle cells (YSMCs), all cells involved in the atherosclerotic process, resulting in the production of pro-inflammatory cytokines and reactive oxygen species (ROS), thus, enhancing the oxidative stress and, consequently, the inflammatory state underlying atherosclerosis (15,18). Specifically, the infection of monocytes with e. pneumoniae increases adherence of infected monocytes to endothelial cells (15) and triggers the production of pro-inflammatory cytokines, such as IL-I~, IL-6, monocyte chemoattract protein-I (MCP-I), macrophage inflammatory protein la and IL-12 (IS).…”

“…As a result, e. pneumoniae may infect monocytes/macrophages, endothelial cells and vascular smooth muscle cells (YSMCs), all cells involved in the atherosclerotic process, resulting in the production of pro-inflammatory cytokines and reactive oxygen species (ROS), thus, enhancing the oxidative stress and, consequently, the inflammatory state underlying atherosclerosis (15,18). Specifically, the infection of monocytes with e. pneumoniae increases adherence of infected monocytes to endothelial cells (15) and triggers the production of pro-inflammatory cytokines, such as IL-I~, IL-6, monocyte chemoattract protein-I (MCP-I), macrophage inflammatory protein la and IL-12 (IS). Moreover, e. pneumoniae has been observed to induce low density lipoprotein (LDL) oxidation and intake in macrophages, promoting foam cell formation (15,19).…”

Lack of strong association of Chlamydia pneumoniae and atherosclerosis in a Jordanian population

“…C. pneumoniae was also found to elicit inflammatory cytokines, inducing chronic inflammation [15]. Furthermore, C. pneumoniae has been shown to induce foam cell formation, smooth muscle cell multiplication, platelet aggregation, and production of reactive oxygen intermediates and cellular adhesion molecules [15,16]. Paradoxically, other in vivo and in vitro studies have failed to link C. pneumoniae with atherosclerosis [17] and, therefore, it remains controversial whether C. pneumoniae could actively play a role in vascular disease development or is an innocent bystander.…”