Sylvie Girard

TL;DR: It is demonstrated that end of gestation exposure of pregnant rats to systemic microbial product (LPS) triggers placental inflammation and massive cell death, fetal mortality, and both forebrain white matter and motor behavioral alterations in the offspring, suggesting a possible protective treatment against human placental and fetal brain damage.

TL;DR: It is shown that both BV2‐microglia and mouse bone marrow derived macrophages were able to adopt different phenotypes after LPS (M1) or IL‐4 (M2) treatment in vitro, but regulated cell death differently when added to mouse organotypic hippocampal brain slices, suggesting macrophage infiltrating the brain from the periphery after an injury may be cytotoxic, independently of their phenotype, while microglia may be protective.

TL;DR: HI and LPS+HI induce pro-inflammatory oriented immune responses in both preterm and term like brains, with a maximal inflammatory response triggered by the combination of L PS+HI, and striking variations according to age are presented.

TL;DR: It is suggested that haem, released from lysed red blood cells in the subarachnoid space, acts as a danger-associated molecular pattern (DAMP) driving IL-1-dependent inflammation.

TL;DR: It is shown that exposure to lipopolysaccharide (LPS) or hypoxia-ischemia (H/I) induced behavioral alterations in animals subjected to forced motor activity and motor deficits reached their highest intensity and affected both spontaneous and forced motor activities.