Pregnant women and children are most vulnerable to malarial infection. Malaria in pregnancy leads to intrauterine growth restriction and preterm deliveries, resulting in low birth weight babies. The underlying mechanisms that lead to these poor birth outcomes are not well understood, but it is known that severe inflammation in the placenta together with excessive fibrin deposition are common features of placental malaria, and correlate with low birth weight. These inflammation and coagulation processes in the placenta occur as an immunological response to the malaria infection. This study addresses the hypothesis that local malaria-induced inflammatory responses induce placental coagulopathy, which is turn leads to significant compromise in placental function, and therefore, fetal distress. This study will mainly focus on the role of coagulation and immunological factors in the disease response process of mice. Murine placental malaria has proven to be an effective model for P. falciparum infection in humans. Mouse RNA has been isolated, and primers for each coagulation factor have been developed. Using these primers and isolated RNA, the next step will be to conduct real time PCR to determine possible upregulation of the coagulation factors. Further research possibilities include determining whether fetal or maternal cells initiate this immunological response leading to inflammation and coagulation in the placenta. Identifying the role of coagulation factors involved in the immunological response to placental malaria will provide further understanding on malarial pathogenesis and ways to prevent fetal growth restriction.