With further in vivo and in vitro verification in response to infection, we revealed that meningitic E. coli-induced IL-17A significantly down-regulated the expression of TJs and AJs of hBMECs at the post-transcriptional level through inhibiting PRTN3/PAR-2 axis, thus augmenting endothelial permeability and disrupting BBB integrity. The gene discussed is PRTN3; the disease is infection.