Chlamydia Pneumoniae Infections and Atherosclerosis Mechanisms

Chlamydia pneumoniae is an obligate intracellular bacterium traditionally associated with respiratory tract infections but increasingly implicated in the development and progression of atherosclerosis. After inhalation and initial pulmonary colonisation, the pathogen can disseminate via infected monocytes and lymphocytes to vascular tissues, where it persists within endothelial cells, vascular smooth muscle cells and macrophages. Persistent infection triggers chronic low‐grade inflammation, characterised by elevated cytokines and adhesion molecules, and promotes oxidative stress through enhanced production of reactive oxygen species. Alterations in lipid handling and membrane microdomains facilitate monocyte adhesion and transmigration into the intima, where foam cell formation and extracellular matrix remodelling drive plaque initiation and growth. Vascular smooth muscle cell migration and proliferation further contribute to plaque complexity and instability. These interwoven processes underscore a paradigm in which infectious burden acts in concert with traditional risk factors such as hyperlipidaemia and hypertension, pointing to novel anti‐infective and antioxidant strategies as potential adjuncts to lipid‐lowering and anti‐inflammatory therapies.

Research from Nature Portfolio

Seminal work has demonstrated that C. pneumoniae infection profoundly alters the biophysical properties of circulating monocytes, reducing membrane cholesterol content, increasing fluidity and disrupting lipid raft organisation. These changes redistribute key adhesion receptors such as CD44 and slow monocyte rolling on endothelial surfaces, thereby strengthening firm adhesion under physiological shear stress. The presence of low‐density lipoprotein further amplifies adhesion, offering a mechanistic link between hyperlipidaemia and enhanced recruitment of infected monocytes to nascent atherosclerotic foci. This framework provides a quantifiable basis for assessing the role of infectious burden in plaque initiation and progression.

Chlamydia Pneumoniae Infections and Atherosclerosis Mechanisms publication trend

The graph below shows the total number of articles in chlamydia pneumoniae infections and atherosclerosis mechanisms across all publications each year (not limited to Nature Index journals).

Technical terms

Atherosclerosis: Chronic inflammatory disease characterised by lipid accumulation, immune cell infiltration and fibrous cap formation within the arterial wall.

Lipid rafts: Cholesterol‐enriched microdomains in the plasma membrane that organise receptor signalling and adhesion molecule distribution.

Foam cell: Lipid‐laden macrophage within atherosclerotic plaques, formed by uptake of modified low‐density lipoprotein.

Reactive oxygen species (ROS): Chemically reactive molecules derived from oxygen, which can cause oxidative damage and modulate signalling pathways.

Vascular smooth muscle cell (VSMC): Contractile cell in the arterial media that can migrate and proliferate during plaque development.

Toll-like receptor 2 (TLR2): Innate immune receptor that recognises bacterial components and mediates pro-inflammatory signalling.

References

1. Biophysical regulation of Chlamydia pneumoniae-infected monocyte recruitment to atherosclerotic foci. Scientific Reports (2016).
2. Chlamydia pneumoniae‐Mediated Inflammation in Atherosclerosis: A Meta‐Analysis. Mediators of Inflammation (2015).
3. Mycoplasma pneumoniae and/or Chlamydophila pneumoniae inoculation causing different aggravations in cholesterol-induced atherosclerosis in apoE KO male mice. BMC Microbiology (2009).
4. Chlamydia pneumoniae Infection Exacerbates Atherosclerosis in ApoB100only/LDLR−/− Mouse Strain. BioMed Research International (2018).
5. Chlamydia pneumoniae Infection Induces Vascular Smooth Muscle Cell Migration and Atherosclerosis Through Mitochondrial Reactive Oxygen Species-Mediated JunB-Fra-1 Activation. Frontiers in Cell and Developmental Biology (2022).