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Is there a role for bradykinin in cerebral malaria pathogenesis?

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FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2023.1184896

Keywords

cerebral malaria; bradykinin; factor XII; prekallikrein; high molecule weight kininogen; bradykinin B2 and B1 receptors

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Malaria is a parasitic disease that is globally significant, especially in endemic regions, and is a major cause of death in children. The mechanisms of cerebral malaria, particularly the role of bradykinin, are not fully understood, but recent discoveries suggest its potential involvement in the disease.
Malaria is a parasitic disease of global health significance and a leading cause of death in children living in endemic regions. Although various Plasmodium species are responsible for the disease, Plasmodium falciparum infection accounts for most severe cases of the disease in humans. The mechanisms of cerebral malaria pathogenesis have been studied extensively in humans and animal malaria models; however, it is far from being fully understood. Recent discoveries indicate a potential role of bradykinin and the kallikrein kinin system in the pathogenesis of cerebral malaria. The aim of this review is to highlight how bradykinin is formed in cerebral malaria and how it may impact cerebral blood-brain barrier function. Areas of interest in this context include Plasmodium parasite enzymes that directly generate bradykinin from plasma protein precursors, cytoadhesion of P. falciparum infected red blood cells to brain endothelial cells, and endothelial cell blood-brain barrier disruption.

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