Atherosclerosis is an inflammatory disease where activated cells are involved in its initiation and progression. Guha and Mackman (32) have shown that activated TLR4 elicits the production of inflammatory cytokines and chemokines. Edfeldt et al. (33) have also found that TLR4 is prominently expressed in endothelial cells of human atherosclerotic lesion, but poorly expressed in normal human arteries. In the early atherosclerotic lesion, LPS and other ligands can stimulate the TLR4 expression on macrophages. The activated receptors can then initiate the signaling cascade that induces the expression of inflammatory cytokines, proteases, and cytotoxic oxygen and nitrogen radicals. These entities further speed up the progression of the atherosclerotic lesion (34) . In advanced atherosclerotic lesion, LPS can induce the proliferation of vascular smooth muscle cells, as well as the expression of elastin-degrading enzyme via TLR4 (35) . Besides that, in response to chemokines, more smooth muscle cells will also migrate to the sites of the lesions (36). These predominant changes cause the accumulation of cells, extracellular matrix components, thickening of the intima, as well as the deformity of the arterial wall.