This novel concept was shown by our demonstrations (a) that S1P levels were significantly increased in HBMEC in response to meningitic E. coli infection, (b) that SphK2 inhibitors, but not SphK1 inhibitors, and S1P2 antagonist, but not S1P1/3 antagonist, inhibited E. coli invasion of HBMEC and (c) that the E. coli factors contributing to EGFR activation (OmpA, FimH, NlpI) were also shown to be involved in the activation of SphK2, and subsequent S1P generation in response to E. coli RS218. This evidence concerns the gene SPHK2 and escherichia coli infection.