Gretta Smith

Introduction. Preeclampsia is a serious health condition consisting of hypertension and proteinuria and occurring in 3-7% of pregnancies.⁸ The etiology of the condition has been studied extensively with limited definitive answers, although a link to inflammatory processes has been discovered. This has led to increased research into the role of maternal bacterial and viral infection in the development of preeclampsia. Methods. Researchers have utilized rat models as well as human placental tissue samples in studies to examine the involvement of PAMPs and TLRs in the pathogenesis of infection-associated preeclampsia. Scharfe-Nugent et al., Faas et al., and Tinsley et al. utilized pregnant and non-pregnant rats in their studies of inflammation in pregnancy. Rat models and controls were injected with free fetal DNA, LPS, and poly(I:C), respectively in each study, and physiologic responses were studied at various time intervals.^{5, 9, 10} Human placental tissue samples were genotyped using PCR and Illumina MiSeq platform for presence of bacterial infection.² Results. The results of these studies showed that TLRs and PAMPs both played a role inflammatory processes associated with preeclampsia. Stimulation of TLRs and PAMPs with their ligands in pregnant rats resulted in increased uterine inflammatory response, increased fetal reabsorption, malformed pups, and a statistically significant (p < 0.05) increase in hypertension and proteinuria, while the non-pregnant rats were not affected.^{5, 9, 10} The human placental tissue studies found that bacterial infection was present in 12.7% of samples from women with preeclampsia, and in none of the samples from women without preeclampsia (p = 0.006). Of the women with bacterial infections, it was found that in 71.4% of samples, a single infectious agent accounted for over 90% of the generated sequences.² Conclusions. These results indicate that while not the only factor causing preeclampsia, inflammatory processes resulting from bacterial and viral infections do most likely play a role in the formation of preeclampsia in affected mothers. Due to this, preventative measures to avoid infections in pregnant women are crucial to avoid increased maternal and perinatal mortality. Further research can be done in this field by examining alternative inflammatory pathways, deciphering implications of particular infections, and what role other physiologic and pathologic processes have in producing infection-associated and non-infection associated preeclampsia.

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