Maternal N-acetylcysteine suppresses fetal inflammatory cytokine responses to maternal lipopolysaccharide.

Abstract

Evidence suggests that maternal infections may induce fetal inflammatory responses. Because cytokine actions may be mediated by oxidative stress, we determined whether N-acetylcysteine, an antioxidant, can blunt fetal inflammatory responses to maternal lipopolysaccharide. Sprague Dawley near-term rats (n = 16) received intraperitoneal lipopolysaccharide (100 microg/kg) at 30 minutes and saline solution or N-acetylcysteine (300 mg/kg) at 150 minutes. An additional group received N-acetylcysteine before and after lipopolysaccharide administration. At 6 hours, rats were killed, and fetal and maternal blood cytokines were determined. After maternal lipopolysaccharide administration, fetal blood interleukin-6 markedly increased (3 +/- 2 to 1265 +/- 574 pg/mL); N-acetylcysteine that was given before or before and after lipopolysaccharide administration reduced fetal interleukin-6 response to control levels. A similar trend was observed for interleukin-1beta. No effect of N-acetylcysteine on fetal interleukin-10 levels was observed. Maternal N-acetylcysteine inhibits fetal cytokine responses to maternal lipopolysaccharide, even when given 2 hours after lipopolysaccharide injection. These results suggest that N-acetylcysteine may protect the fetus from sequelae of maternal inflammation.