Moreover, in a mouse model of atherosclerosis (ApoE−/− mice), short-term treatment of lipopolysaccharide (LPS) in a super-low-dose that mimics chronic infection elicits the polarization of monocytes into a sustained pro-inflammatory state with upregulated Ly6C, CCR5, MCP-1, and decreased SR-B1 expression level, and the result of which is the aggravation of atherosclerosis (27). The gene discussed is CCL2; the disease is atherosclerosis.