Studies on mouse models of bacterial meningitis revealed a stronger glial cell marker expression in FPR1-deficient mice and an increase of activated microglial cells and neutrophil infiltration in FPR1- or FPR2-deficient mice, thus suggesting that FPRs exert an important role in the immune responses within the CNS and that the lack of these receptors leads to a dysregulation of the inflammatory response compared with wild-type mice. This evidence concerns the gene FPR2 and bacterial meningitis.