Atherogenetically relevant cells support continuous growth of Chlamydia pneumoniae
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Published on: October 23, 2013
M Maass1, J Gieffers, W Solbach
1Institute of Medical Microbiology and Hygiene, Medical University of Lübeck, Germany. maass@hygiene.mu-luebeck.de
Abstract:
The obligate intracellular bacterium Chlamydia pneumoniae has been implicated in the pathogenesis of atherosclerosis since viable pathogen has been recovered from plaques. Chlamydiae are epithelial pathogens notorious for causing persistent infection. Atherosclerosis, however, is a chronic inflammatory disease involving mesenchymal cells of the vascular wall. A bacterial contribution to atherosclerosis appears more relevant if the resident mesenchymal cells of the vascular wall that constitute the plaque can support chlamydial infection continuously. Therefore we inoculated immortalized and primary mesenchymal cells with a vascular and a respiratory Chlamydia pneumoniae isolate. Primary human coronary artery endothelial and smooth muscle cells, primary human embryonic fibroblasts as well as the immortalized cell lines were permissive for continuous growth of both strains. Thus, the resident vascular cells that produce the atheromatous plaque can acquire permanent productive. Chlamydia pneumoniae infection. Immortalized monocytic cells and peripheral blood monocytes also supported chlamydial growth, though productive infection ceased after 5 passages. Monocytes/macrophages are not resident cells of the vascular wall but have an active role in plaque formation. Systemic circulation and transendothelial migration makes them a potential vector system for chlamydial distribution. These findings add further plausibility to the hypothesis of a chronic infectious component in the multifactorial condition of atherosclerosis. Further studies must precisely define chlamydial target cells in vivo and differentiate infection in resident cells of the vascular wall from a presence limited to migrating macrophages. Endovascular infection might provide an explanation for unclear phenomena of atherogenesis like mesenchymal cell proliferation and its distinct inflammatory component.
Insights
Chlamydia pneumoniae can continuously infect mesenchymal cells in the vascular wall, supporting the hypothesis that this bacterium contributes to atherosclerosis. This finding suggests a potential infectious cause for this chronic inflammatory disease.
Area of Science:
- Microbiology
- Cardiovascular Disease
- Pathogenesis
Background:
- Chlamydia pneumoniae, an obligate intracellular bacterium, has been linked to atherosclerosis due to its presence in plaques.
- Atherosclerosis involves chronic inflammation in vascular wall mesenchymal cells, distinct from Chlamydiae's typical epithelial cell targets.
- Understanding if vascular mesenchymal cells support persistent Chlamydia pneumoniae infection is crucial for its role in atherosclerosis.
Purpose of the Study:
- To investigate the susceptibility of vascular mesenchymal cells to Chlamydia pneumoniae infection.
- To determine if Chlamydia pneumoniae can establish persistent infections in cells relevant to atherosclerosis.
- To explore the potential role of monocytes/macrophages in Chlamydia pneumoniae distribution within the vascular system.
Main Methods:
- Inoculation of immortalized and primary human coronary artery endothelial cells, smooth muscle cells, and fibroblasts with Chlamydia pneumoniae.
- Assessment of Chlamydia pneumoniae growth and persistence in various cell types, including monocytic cells and peripheral blood monocytes.
- Monitoring of productive infection over multiple cell passages.
Main Results:
- Primary and immortalized human vascular mesenchymal cells (endothelial, smooth muscle, fibroblasts) were permissive to continuous Chlamydia pneumoniae growth.
- Both vascular and respiratory Chlamydia pneumoniae isolates established persistent, productive infections in resident vascular cells.
- Monocytic cells and monocytes supported chlamydial growth, but productive infection was limited to 5 passages.
Conclusions:
- Resident vascular cells of the atheromatous plaque can support permanent, productive Chlamydia pneumoniae infections.
- These findings strengthen the hypothesis of a chronic infectious component in atherosclerosis.
- Further research is needed to differentiate in vivo infection in resident vascular cells versus transient infection in migrating macrophages.
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