2Department of Obstetrics and Gynecology, School of Medicine
3Infertility Research Center
4Proteomics Laboratory, School of Advanced Medical Sciences and Technologies
5Autoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
Background: Preeclampsia (PE) is one of the most complex and life-threatening pregnancy disorders and is considered as a major cause of mortality among mothers and fetuses worldwide. Although the exact etiology of PE is not well known several lines of evidence support an immunological etiology for PE. Objective: To investigate the differences in the expression of TLRs 2, 4, 5, and 6 and a group of inflammatory cytokines including IL-1, IL-6, TNF-α and IFN-γ in placentas from PE and healthy pregnant women in their third trimester of pregnancy. Methods: This case-control study was performed on fifteen PE and fifteen age and gestational matched healthy pregnant women in the third trimester of pregnancy. Real time PCR (RT-PCR) technique was used to determine the expression of TLRs 2, 4, 5, and 6 in the maternal and fetal parts of the placenta. Moreover, the expressions of IL-1, IL-6, TNF-α and IFN-γ at RNA level in placental samples, peripheral, and cord blood were investigated. Results: The results of the present study indicated that the expressions of TLRs 4, 5 and 6 were significantly increased in both maternal part (p<0.001 and p<0.003 for TLRs 4, 6 and TLR 5, respectively) and fetal part (p<0.001), while TLR2 showed significant increase only in the fetal part of PE placentas (p<0.002). The levels of all studied cytokines showed over-expression within peripheral and cord blood samples from PE patients (p<0.001 for IL-1, IL-6, and IFN-γ and p<0.004 for TNF-α in both cord and peripheral blood samples). Conclusion: The finding of the present study indicated that the expression of the studied TLRs and inflammatory cytokines are generally suppressed in normal pregnancy, but are up regulated in preeclamptic women. Moreover, it seems that the maternal and fetal parts of the placenta may play different roles in the induction of the inflammatory status within the placenta.