Experiments performed in our laboratory on this model of LPS-induced materno-fetal inflammatory response showed that the interleukin-1 (IL-1) system, and especially the IL-1/IL-1 receptor antagonist (IL-1Ra) ratio played a key role in the pathophysiology of LPS-induced: (i) chorioamnionitis; (ii) macrophagic arteritis within the placenta and the umbilical cord; and (iii) fetal brain injuries [13]. This evidence concerns the gene IL1B and arteritis.