Fig. 2
From: New means to assess neonatal inflammatory brain injury
Proposed mechanisms mediating peripheral inflammation and brain injury. Sepsis can overstimulate TLRs on endothelial (BBB/CVO) and/or epithelial (choroid plexus) cells, which shift resting microglia to pro-inflammatory microglia that induce brain injury. PAM pathogen-associated molecules, Poly:IC polyinosinic: polycytidylic acid, TLR toll-like receptor, LPS lipopolysaccharide, IL interleukin, IL-1R interleukin-1 receptor, TNF tumor necrosis factor, NO nitric oxide, PGE 2 prostaglandin E2