These findings together reveal that miR-19b-3p itself could act to amplify the neuroinflammatory responses at the BBB, and when suffering from meningitic E. coli infection, the host could in turn initiate an effective “quenching mechanism” by attenuating miR-19b-3p/TNFAIP3/NF-κB signaling, which results in alleviation of the proinflammatory responses induced by bacteria at the entry of the BBB. This evidence concerns the gene TNFAIP3 and escherichia coli infection.