Serum of cytomegalovirus-infected mice induces monocyte chemoattractant protein-1 expression by endothelial cells

Inflammation plays a central role in atherogenesis. It was hypothesized tha t infection of apolipoprotein E-deficient mice with murine cytomegalovirus (MCMV) increases serum levels of proinflammatory cytokines, which may induc e "proatherosclerotic" changes in endothelial cells (ECs). Serum samples we re collected from uninfected and infected mice. ELISA was used to determine cytokine serum levels and monocyte chemoattractant protein-1 (MCP-1) level s in the supernatant of mouse ECs incubated with serum-containing medium. S erum samples from infected mice induced MCP-1 expression by ECs. These seru m samples contain interferon (IFN)-gamma, whereas IFN-gamma was undetectabl e in serum samples from uninfected mice. Preincubating infected mouse serum with anti-IFN-gamma monoclonal antibody significantly decreased serum-indu ced EC expression of MCP-1. Thus, MCMV infection increases IFN-gamma serum levels, such serum can induce MCP-1 in ECs, and the serum-induced MCP-1 exp ression is due, at least in part, to IFN-gamma. If these changes in EC func tion also occur in vivo in response to infection, they could exacerbate ath erogenesis.