Attivazione delle vie immunitarie dell'ospite in risposta all'infezione del parassita Trypanosoma brucei

African trypanosomes are pathogenic parasites that cause a variety of diseases in humans and animals. Infections by these parasites are a major health and economic burden in sub-Saharan Africa. One neglected aspect of infection is the immune response triggered in gravid hosts. The placenta is a critical organ for the development of the fetus, and it is important to understand how it responds to the presence of parasites. The goal of this study was to elucidate specific immune pathways triggered in the placenta by a trypanosome infection. BeWo cells are a human placental trophoblast cell line that are known to be susceptible to infection by T. brucei. To determine this, cultured BeWo cells were exposed to parasites, simulating a short or long-term infection. Activation of immune pathways in host cells was quantified using qPCR to determine fold changes in targeted immune pathway effectors. The results of this study showed BeWo cells in culture produced increased levels of the inflammatory cytokines TNF-α, IL-1α, and no response of IFN-γ in response to the presence of T. brucei. These pathways are important for the clearance of parasites and the protection of the fetus. The study also found that the addition of 80:20 media, which is a mixture of DMEM F12 and HMI9 media, to BeWo cells in culture further increased the production of these inflammatory cytokines. The findings of this study provide new insights into the immune response to African trypanosomes in the placenta. These findings suggest that the presence of T. brucei can induce an inflammatory response in BeWo cells. This inflammatory response may contribute to the pathogenesis of HAT (Human African Trypanosomiasis). The study also suggests that the addition of 80:20 media to BeWo cells in culture may further increase the inflammatory response. This finding may have implications for the development of new strategies for the prevention and treatment for HAT.