Involvement of PKCα–MAPK/ERK-phospholipase A2 pathway in the Escherichia coli invasion of brain microvascular endothelial cells

Escherichia coli K1 is the most common Gram-negative organism that causes neonatal meningitis following penetration of the blood–brain barrier. In the present study we demonstrated the involvement of cytosolic (cPLA2) and calcium-independent phospholipase A2 (iPLA2) and the contribution of cyclooxygenase-2 products in E. coli invasion of microvascular endothelial cells. The traversal of bacteria did not determine trans-endothelial electrical resistance (TEER) and ZO-1 expression changes and was reduced by PLA2s siRNA. cPLA2 and iPLA2 enzyme activities and cPLA2 phosphorylation were stimulated after E. coli incubation and were attenuated by PLA2, PI3-K, ERK 1/2 inhibitors. Our results demonstrate the role of PKCα/ERK/MAPK signaling pathways in governing the E. coli penetration into the brain.

► Brain microvascular endothelial cells invasion by E. coli.
► PLA2s and COX-2 involvment.
► PKCα/ERK/MAPK signaling pathway govern the E. coli penetration into the brain.