Severe malaria (SM) places a disproportionate burden of nriortality and death on the children of Sub-Saharan Africa. Death, as a result of SM, is not a direct consequence of parasite load but is associated with excessive inflammatory response(s) in the brain and lungs of SM patients. Parasite-derived activators of the innate immune response, together with inflammatory monocytes, have been implicated in mediating this tissue damage. However, the activation pathways responsible for localized inflammation and compromising the blood brain barrier (BBB) remain to be determined. We propose elucidating the mechanism(s) by: 1. Defining the transcriptional profiles at the sites of damage in tissues from pediatric SM. We propose assembling a transcriptional
90% of the deaths caused by severe malaria occur in children in Sub-Saharan Africa. Death, most frequently, is the result of an inappropriate level of inflammation in the microvasculature of the brain or the lungs of the SM patient. This project proposes determination of the role of parasite pigment-loaded monocytes in mediating or exacerbating this pathology, and the identification of chemotherapeutic approaches to de-activate the damaging cellular response. the identification of chemotherapeutic
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