Fig. 10From: Meningitic Escherichia coli α-hemolysin aggravates blood–brain barrier disruption via targeting TGFβ1-triggered hedgehog signalingSchematic presentation of the TGFβ1-mediated intercellular communication for maintaining the normal BBB function as well as the disturbance by meningitic E. coli for the BBB disruption. Without infection, astrocytes-derived TGFβ1 physiologically triggered the TGFβ1-TGFBRII-Smad2/3-Gli1/2-ZO-1 axis in BMECs to maintain the normal BBB function (left panel). Upon meningitic E. coli infection, bacterial virulence determinant α-hemolysin effectively helped to disturb this functional cross-talking between astrocytes and BMECs by attenuating both TGFβ1 receptor TGFBRII as well as the hedgehog signaling transcription factors Gli1/2 in BMECs, thus led to the BBB dysfunctionBack to article page