Table 2.
Summary of pro atherosclerotic mechanisms in chronic infections and TLRs involved
| Pathogen | Phase of atherogenesis | TLRs involved |
|---|---|---|
| C. pneumoniae | Activation of endothelium | TLR2 |
| Migration of leucocytes | TLR4 | |
| Lesion rupture | ||
| Thrombosis | ||
| P. gingivalis | Activation of endothelium | TLR2 |
| Formation of lipid core | TLR4 | |
| Proliferation of SMCs | ||
| H. pylori | Activation of endothelium | TLR2 |
| Macrophage derived foam cell formation | TLR4 | |
| Lesion instability | TLR5 | |
| TLR9 | ||
| HIV | Activation of endothelium | TLR3 |
| Formation of lipid core | TLR4 | |
| Lesion rupture | TLR7 | |
| TLR8 | ||
| CMV | Activation of endothelium | TLR2 |
| Migration of leucocytes | TLR7 | |
| Proliferation of SMCs | TLR9 | |
| Lesion rupture | ||
| Thrombosis | ||
| HSV | Thrombosis | TLR2 |
| TLR3 | ||
| TLR7 | ||
| TLR9 |
Summary of the aspects of pathogens affecting the development of atherosclerosis and the TLRs involved in each pathogen
TLRs toll like receptors, C. pneumoniaeChlamydia pneumonia, P. gingivalisPorphyromonas gingivalis, H. pyloriHelicobacter pylori,HIV human immunodeficiency virus, CMV Cytomegalovirus, HSV herpes simplex virus