C3aR is up-regulated in glial cells and infiltrating immune cell populations in the brain tissue autopsy from bacterial meningitis patients (Gasque et al., 1998), and C5aR deficient mice were less susceptible to meningitis development despite unaltered bacterial titers in the brain (Woehrl et al., 2011), suggesting the important roles for anaphylatoxin receptor signaling in infection-induced neuroinflammation. This evidence concerns the gene C3AR1 and infection.