Toll-Like Receptor 2 Mediates Persistent Chemokine Release by Chlamydia pneumoniae –Infected Vascular Smooth Muscle Cells
- 1 November 2005
- journal article
- research article
- Published by Ovid Technologies (Wolters Kluwer Health) in Arteriosclerosis, Thrombosis, and Vascular Biology
- Vol. 25 (11), 2308-2314
- https://doi.org/10.1161/01.atv.0000187468.00675.a3
Abstract
Objective— The intracellular bacterium Chlamydia pneumoniae is present in many atherosclerotic lesions, where it could promote inflammation. This study determined whether monocyte chemoattractant protein 1 (MCP-1) release is stimulated in vascular smooth muscle cells (VSMCs) that are exposed to or infected by C pneumoniae and whether toll-like receptor 2 (TLR2) or TLR4 mediate these effects. Methods and Results— TLR2 mRNA was expressed constitutively and was upregulated by C pneumoniae exposure in mouse aortic SMC and was inducible by C pneumoniae and TLR3 and TLR4 agonists in human coronary artery SMCs. Exposure to inactivated or viable extracellular C pneumoniae evoked a robust increase in MCP-1 release and activated nuclear factor-κB and extracellular signal–regulated kinase 1/2 in wild-type and TLR4 signaling–deficient mouse aortic SMCs but not in TLR2-deficient SMCs, probably because of TLR2-mediated recognition of a chlamydial antigen. Brief exposure to viable C pneumoniae led to active infection of VSMCs, shown by chlamydial protein synthesis, and caused a persistent (>48-hour) MCP-1 release that was also TLR2 dependent. Conclusions— The results show that VSMCs express functional TLR2 and that TLR2 mediates both a persistent activation of chemokine release in C pneumoniae –infected VSMCs and its acute stimulation by extracellular C pneumoniae . Therefore, TLR2 expressed in VSMCs may promote inflammation within the arterial wall.Keywords
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