Prolactin levels declined in the presence of IL-ip plus indomethacin (p < 0.05).
The prolactin levels of the 5 animals treated with IL-1 Э plus indomethacin were stratified into three time periods for statistical analysis, and the results are shown in Figure 5, A and B. There was a significant decline in prolactin immediately after infusion that was maintained to 72 h. These results are similar to the results obtained with IL-lfi alone.
Figure 6 illustrates areas of the choriodecidua from a full-term control pregnancy and experimental group В streptococcal chorioamnionitis in rhesus monkeys. Both experimental streptococcal infection and intraamniotic IL-ip infusion resulted in acute exudative chorioamnionitis characterized by segmental or continuous laminar infiltration of neutrophils into dense chorionic connective tissue, extra-villous trophoblasts, and superficial parietal decidua juxtaposed to the trophoblast-decidual interface. Inflammatory cell infiltration was accompanied by edema and collagen fiber disarray in the dense chorionic connective tissue and necrosis of extra villous trophoblastic cells. Interstitial edema accompanied neutrophil infiltration in the superficial decidua, but decidual cell necrosis was minimal and was confined to localized areas adjacent to focal chorionic neutrophilic infiltration. The amnion and deeper decidua were generally unaffected. The qualitative and quantitative features of experimental group В streptococcal chorioamnionitis were similar regardless of the route of infection. Chorioamnionitis resulting from intraamniotic administration of IL-1 (3 was indistinguishable from group В streptococcal infection with the exception that leukocytic infiltrates in the chorion tended to be diffuse with less decidual involvement. Indomethacin treatment appeared to have no effect on the histologic inflammatory response induced by IL-1 p. buy flovent inhaler
FIG. 4. A) Temporal relationship between IL-1|3 infusion and amniotic fluid concentrations of prolactin for a single representative animal (#12870) following intraamniotic infusion of 10 (xg of IL-1J5. Amniotic fluid prolactin declined from a preinfusion concentration of 104.9 jjLg/ml to 30.2 (Ag/ml by 36 h after infusion. B) Temporal relationship between IL-1 p plus indomethacin infusion and amniotic fluid concentrations of prolactin for a single representative animal (#10401) following 2 days of maternal oral treatment with indomethacin (50 mg twice daily) and intraamniotic infusion of 10 jjLg of IL-1 p. Amniotic fluid prolactin declined from a preinfusion concentration of 57.4 (xg/ml to 33.6 jJLg/ml by 36 h after infusion.
FIG. 5. Summary of the mean (± SEM) amniotic fluid prolactin concentrations following experimental intrauterine infusion of IL-ip alone and IL-1|3 plus indomethacin. The numbers in parentheses indicate the number of animals still undelivered in which samples were obtained at the indicated time. There was a 42% decrease in amniotic fluid prolactin between 0 and 24 h after infusion of IL-1 Э alone (p < 0.05) and a 66% decrease between 24 and 72 h after infusion of IL-1 p alone (p < 0.05). There was a 41% decrease in amniotic fluid prolactin between 0 and 24 h after infusion of IL-1 p plus indomethacin (p < 0.05) and a 50% decrease between 24 and 72 h after infusion of IL-1 p plus indomethacin (p < 0.05). Comparisons were made to baseline prolactin concentrations immediately prior to infusion by ANOVA and Student-Newman-Keuls pairwise comparison. There was no statistical difference between results for IL-ip alone and those for IL-ip plus indomethacin. Closed bars represent IL-1 p alone. Open bars represent IL-ip plus indomethacin. * Significantly different from baseline atp < 0.05. # Significantly different from Time 0-24 h at p < 0.05.
FIG. 6. Microscopic appearance of (top panel; a) normal 159-day gestational age rhesus macaque placental membrane and (bottom panel; b) a 140-day gestational age rhesus macaque placental membrane at 72 h following experimental choriodecidual GBS infection. Experimental streptococcal chorioamnionitis is characterized by acute neutrophil infiltration and edema involving the dense chorionic connective tissues (C), extra-villous trophoblastic cells (T), and superficial decidua parietalis (D) juxtaposed to the decidual-trophoblast interface (arrowheads). Extensive ex-travillous trophoblast necrosis accompanies the inflammatory response. Neutrophils infiltrate the superficial decidua; however, decidual cell necrosis is minimal. Stained with hematoxylin and Lee; bar = 50 |xm.