Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.04.236745v1?rss=1 Authors: Reginatto, M. W., Fontes, K. N., Monteiro, V. S., Liacone, N., Andrade, C. B., Gomes, H. R., Imperio, G. E., Bloise, F. F., Kluck, G., Atella, G., Matthews, S., Bloise, E., Ortiga-Carvalho, T. M. Abstract: There is growing evidence that infection impacts the expression of transporters that mediate placental exchange of xenobiotics, lipids and cytokines. We hypothesized that lipopolysaccharide (LPS), modifies the expression of placental transport systems and lipid homeostasis. LPS (150 [mu]g/Kg;ip.) treatments were conducted for 4h or 24h and animals were euthanized at gestational-days (GD) 15.5 or 18.5 and maternal blood, fetuses and placentae collected. Increased rates of fetal demise were observed at GD15.5 following LPS, whereas at GD18.5, high rates of early labor occurred; associated with distinct pro-inflammatory responses. LPS decreased placental Fabppm at GD15.5 (LPS-4h); increased Fat/Cd36 at GD18.5 (LPS-4h) and reduced Abcb1b, Abcc2 and Abcc5 at GD18.5 (LPS-24h). At the level of protein, breast cancer-related protein (BCRP) and Abcg1 were decreased in the labyrinth (L) at both time-points, whereas P-glycoprotein (P-gp) in the L was decreased at GD18.5. Specific maternal plasma and placental changes in triacylglycerol, free fatty acids, cholesterol, cholesterol ester and monoacylglycerol were detected in a gestational-age dependent manner. In conclusion, LPS associated with increased fetal death and early labor decreased placental ABC transporter expression and altered maternal plasma and placental lipid homeostasis. These changes likely modify fetal xenobiotic exposure and placental lipid exchange in cases of bacterial infection. Copy rights belong to original authors. Visit the link for more info