We have demonstrated that Brucella infects and survives within human synoviocytes, and this infection elicits a proinflammatory microenvironment with the secretion of interleukin (IL)-6 and the chemokines IL-8; chemoattractant of neutrophils and monocyte chemoattractant protein 1 (MCP-1); chemoattractant of monocytes; and the secretion of matrix metalloproteases (MMPs) and RANKL—with concomitant osteoclastogenesis (7, 8). Here, CCL2 is linked to infection.