OBJECTIVE: The aim of this study was to characterize the pregnant guinea pig cytokine time course following a maternal inflammatory insult. STUDY DESIGN: Pregnant guinea pigs (n = 34) were injected intraperitoneally with 100 microg/kg lipopolysaccharide (LPS) at 70% gestation and euthanized at 24 hours, 48 hours, or 5 days. Control animals were euthanized at 70% gestation without LPS exposure. Interleukin (IL)-6, IL-1beta, and tumor necrosis factor-alpha (TNF-alpha) were quantified in the maternal serum and amniotic fluid by an enzyme-linked immunosorbent assay. RESULTS: IL-6 and IL-1beta concentrations were elevated in the maternal serum at 24 hours and returned to control levels by 5 days. In the amniotic fluid, IL-6 peaked at 48 hours and IL-1beta at 24 hours. TNF-alpha levels were not significantly increased. CONCLUSION: Maternal intraperitoneal LPS injection produces transient increases in cytokine concentrations in the maternal serum and amniotic fluid within 5 days, further implicating the cytokines as mediators of fetal white matter damage.
OBJECTIVE: The aim of this study was to characterize the pregnant guinea pig cytokine time course following a maternal inflammatory insult. STUDY DESIGN: Pregnant guinea pigs (n = 34) were injected intraperitoneally with 100 microg/kg lipopolysaccharide (LPS) at 70% gestation and euthanized at 24 hours, 48 hours, or 5 days. Control animals were euthanized at 70% gestation without LPS exposure. Interleukin (IL)-6, IL-1beta, and tumor necrosis factor-alpha (TNF-alpha) were quantified in the maternal serum and amniotic fluid by an enzyme-linked immunosorbent assay. RESULTS:IL-6 and IL-1beta concentrations were elevated in the maternal serum at 24 hours and returned to control levels by 5 days. In the amniotic fluid, IL-6 peaked at 48 hours and IL-1beta at 24 hours. TNF-alpha levels were not significantly increased. CONCLUSION: Maternal intraperitoneal LPS injection produces transient increases in cytokine concentrations in the maternal serum and amniotic fluid within 5 days, further implicating the cytokines as mediators of fetal white matter damage.