Altered hepatic inflammatory response in the offspring following prenatal LPS exposure.

There is increasing evidence that maternal immune activation has a significant impact on the offspring's immune function. In this study, we examined the effects of maternal immune activation on the offspring's hepatic inflammatory response. We treated pregnant rats with 500 microg/kg LPS or saline on day 18 of pregnancy, subsequently stimulated the offspring with 250 microg/kg LPS or saline at postnatal day (P) 21, and then examined the expression of LPS cell surface receptors, namely toll-like receptor (TLR)-4 and CD14, and cytokines, namely tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6, as well as the activation of key intracellular mediators of the TLR-4 signaling cascade, namely p38 MAPK and p42/44 MAPK, in the offspring liver.

Effects of maternal exposure to LPS on the inflammatory response in the offspring.

To investigate the effects of maternal infection on the offspring's inflammatory response, pups born to LPS- or saline-treated dams were stimulated with LPS or saline, and the expression of cytokines and chemokines was examined. We found that at P21, pups born to LPS-treated dams exhibited diminished serum levels of TNF-alpha, IL-1beta, and IL-6, and inhibited mRNA levels of cytokines, including TNF-alpha, IL-1beta, and IL-6, and chemokines, including MIP-1beta, MIP-2, and KC, in the brain, as compared to pups born to saline-treated dams at 2 h following LPS stimulation. Our results suggest that maternal infection suppresses the offspring's inflammatory response to LPS.