Sylvie Girard1, Luc Tremblay, Martin Lepage, Guillaume Sebire. 1. Laboratoire de Neurologie Pédiatrique, Département de Pédiatrie, Faculté de Médecine et des Sciences de lSanté, Université de Sherbrooke, Sherbrooke, Quebec, Canada. sylvie.girard@manchester.ac.uk
Abstract
OBJECTIVE: We studied whether magnetic resonance imaging (MRI) could be used to detect placental inflammation before the detection of irreversible tissue damage. Next, we tested whether this early detection would enable the administration of treatment (ie, interleukin-1 receptor antagonist [IL-1Ra]) in a realistic clinical time after diagnosis. STUDY DESIGN: Pregnant rats were injected intraperitoneally with lipopolysaccharide with/without delayed IL-1Ra. MRI was performed at different time after the injection, and placentas were collected for comparison. Placental inflammation was assessed by determination of the levels of inflammatory cytokines. RESULTS: Placental inflammation was detected by MRI as early as 3 hours after maternal administration of lipopolysaccharide, concomitantly to IL-1β up-regulation. This was observed before any tissue damage, which appeared only at 24 hours after the administration of lipopolysaccharide. Delayed IL-1Ra administration (after MRI diagnosis) protected the placenta, as seen by the preserved tissue integrity and limited macrophages infiltration in the placental parenchyma. CONCLUSION: These findings established a noninvasive diagnostic method for early in utero detection of placental inflammation that would allow the administration of placentoprotective intervention within a clinically relevant delay after diagnosis.
OBJECTIVE: We studied whether magnetic resonance imaging (MRI) could be used to detect placental inflammation before the detection of irreversible tissue damage. Next, we tested whether this early detection would enable the administration of treatment (ie, interleukin-1 receptor antagonist [IL-1Ra]) in a realistic clinical time after diagnosis. STUDY DESIGN: Pregnant rats were injected intraperitoneally with lipopolysaccharide with/without delayed IL-1Ra. MRI was performed at different time after the injection, and placentas were collected for comparison. Placental inflammation was assessed by determination of the levels of inflammatory cytokines. RESULTS: Placental inflammation was detected by MRI as early as 3 hours after maternal administration of lipopolysaccharide, concomitantly to IL-1β up-regulation. This was observed before any tissue damage, which appeared only at 24 hours after the administration of lipopolysaccharide. Delayed IL-1Ra administration (after MRI diagnosis) protected the placenta, as seen by the preserved tissue integrity and limited macrophages infiltration in the placental parenchyma. CONCLUSION: These findings established a noninvasive diagnostic method for early in utero detection of placental inflammation that would allow the administration of placentoprotective intervention within a clinically relevant delay after diagnosis.
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