The neutralization of CX3CL1/CX3CR1 or CCL2/CCR2 chemokine axes partly inhibits leukocyte adhesion through impaired proinflammatory monocyte (Mon1) adhesiveness to the dysfunctional endothelium, which suggests a potential link between the systemic inflammatory response and CVD development in metabolic syndrome. Here, CCL2 is linked to metabolic syndrome.