Here, by analyzing chemokine production and migration at 24 hours of coculture we majorly focused on the first steps of monocyte/ macrophage activation once they have interacted with trophoblast and PAMPs stimuli. In fact, after 48 hours we have observed increased monocyte migration as previously reported. On this basis, it is conceivable that restraint in monocyte recruitment would serve as an early strategy, then according to the concentration and nature of the PAMP stimulus this restraint could break and leukocytes would be attracted to the interface with subsequent tissue damage and embryo loss. Another interesting point is that poly increased monocyte migration toward Swan-71 cells at 24 h, an effect not seen with LPS or PGN, whereas chemokine MDL-12,330A hydrochloride expression in monocytes or trophoblast cells was not decreased with poly as it was seen with LPS or PGN, suggesting that poly has the ability to bypass the initial restraint strategy. The differential effect might be explained by the diverse downstream signaling events and adapter molecules involved in each TLR/ligand system. Accordingly, Koga et al. have reported that poly Nifurtimox induces preterm delivery in a TLR3-dependent manner in C57B/6 mice. In this model CCL5 production increased 52 times after the stimulation of trophoblast cells with poly while CCL2 just 2.5 times, reflecting that each stimulus might differentially modulate chemokine expression. In humans, chemokine up-regulation within the maternalplacental compartments is associated with microbial invasion and with an exacerbated inflammatory response. As an example, in the chorioamnionitis, placental inflammatory lesions parallel an increase in CXCL10, CXCL11 and CXCL12 concentrations in maternal plasma. Likewise, in the villitis of unknown etiology, a destructive inflammatory lesion of villous placenta, decidual macrophages appear activated in an inflammatory profile and T helper-1 effector profile is observed. The transcriptome of VUE placentas revealed an increase in a subset of chemokines and their receptors, including CCL5 and CCR5, accompanied by a systemic deregulation of CXC chemokines in maternal and fetal circulation.