Cerebral malaria (CM) is a severe complication of and a leading cause of death due to Plasmodium falciparum infection. CM is\nlikely the result of interrelated events, including mechanical obstruction due to parasite sequestration in the microvasculature,\nand upregulation ofTh1 immune responses. In parallel, blood-brain-barrier (BBB) breakdown and damage or death of microglia,\nastrocytes, and neurons occurs.We found that a novel formulation of a liposome-encapsulated glucocorticosteroid, ????-methasone\nhemisuccinate (nSSL-BMS), prevents experimental cerebralmalaria (ECM) in amurine model and creates a survival time-window,\nenabling administration of an antiplasmodial drug before severe anemia develops. nSSL-BMS treatment leads to lower levels of\ncerebral inflammation, expressed by altered levels of corresponding cytokines and chemokines. The results indicate the role of\nintegrated immune responses inECMinduction and showthat the newsteroidal nanodrug nSSL-BMS reverses the balance between\ntheTh1 and Th2 responses in malaria-infected mice so that the proinflammatory processes leading to ECM are prevented. Overall,\nbecause of the immunopathological nature of CM, combined immunomodulator/antiplasmodial treatment should be considered\nfor prevention/treatment of human CM and long-term cognitive damage.
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