Chlamydia pneumoniae-induced pathological signaling in the vasculature

Abstract

Since its description in 1986, Chlamydia pneumoniae has remained one of the most enigmatic pathogens. This intracellular bacterium is highly seroprevalent, but rarely recovered from cell culture, it can genetically switch between a proliferative and a nonreplicative state and has been linked to a vast number of chronic diseases, most notably to atherosclerosis, as it can be found in the plaques. It has become quite clear that persistent bacteria in atherosclerotic lesions cannot be eradicated by currently available antibiotic treatments and that attempts to do so without a better understanding of the pathobiology of chlamydial persistence are futile. However, there is growing knowledge on how vascular chlamydial infection may lead to the pathological reprogramming of the host cell signaling pathways. Chlamydia pneumoniae is now well known to induce, at least in vitro, the two pathogenetic main events that define atherosclerosis: angiogenesis and inflammation. In vivo a contribution of chlamydial infection to the progression of atherosclerosis remains unproven. This minireview provides a brief overview on the proproliferative and proinflammatory effects of vascular C. pneumoniae infection and their potential link to atherogenesis.

Chronic Chlamydial Diseases: From Atherosclerosis to Urogenital Infections

“…In response to infection with C. pneumoniae, acute phase proteins enhance progression and destabilization of atherosclerotic plaques [76]. C. pneumoniae can induce proliferation of vascular smooth muscle cells (VSMCs) and stimulate production of numerous pro-inflammatory mediators and adhesion molecules in VSMCs and endothelial cells [76,78,79]. C. pneumoniae infection can also induce reactive oxygen species (ROS) in macrophages, platelets, endothelial cells and VSMCs, contributing to atherosclerotic lesion development [74].…”

Induction of VEGF and MMP-9 Expression by Toll-like Receptor 2/4 in Human Endothelial Cells Infected withChlamydia Pneumoniae

“…pneumoniae-induced host cell activation and reprogramming is a complex mechanism that involves signaling pathways and several receptor systems of the host cells (4). Using a sensitive flow cytometric technique, we found an increased TLR2/ TLR4 expression on the cell surface of HUVEC.…”

“…Chlamydiae are obligate intracellular pathogens with a specific developmental cycle inside the host cell that have developed unique strategies to promote their intracellular survival (4). Recent findings have shown that the pathogen is able to modulate host cell signaling pathways to ensure either its replication, as in an acute infection, or its prolonged survival in a host cell prevented from undergoing apoptosis (4)(5)(6).…”

“…Recent findings have shown that the pathogen is able to modulate host cell signaling pathways to ensure either its replication, as in an acute infection, or its prolonged survival in a host cell prevented from undergoing apoptosis (4)(5)(6).…”

Estudo biomolecular de produtos de Chlamydophila pneumoniae, Mycoplasma pneumoniae e Borrelia burgdorferi na etiopatogenia da degeneração mixomatosa da valva mitral

“…A disseminação da Chlamydophila pneumoniae pode advir do trato respiratório pelos macrófagos alveolares, que funcionam como vetores promovendo acesso aos vasos sanguíneos [76].…”