CSK and infection: In support of our demonstration that c-Src is downstream of EGFR activation, which is in turn a downstream event of SphK2-S1P-S1P2 signaling in E. coli invasion of HBMEC, we found that pretreatment of HBMEC with the S1P2 antagonist JTE-013 inhibited c-Src activation in response to E. coli RS218 (Fig 5E), while HBMEC pretreated with the c-Src kinase inhibitor PP2 or transfected with the c-Src dominant-negative construct did not affect SphK2 and EGFR activation in response to RS218 infection in HBMEC (Fig 5F and 5G).