Electron microscopic features of brain edema in rodent cerebral malaria in relation to glial fibrillary acidic protein expression |
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Authors: | Sumate Ampawong Urai Chaisri Parnpen Viriyavejakul Apichart Nontprasert Georges E Grau Emsri Pongponratn |
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Institution: | 1.Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, 420/6, Ratchawithi Road, Ratchathewi, Bangkok, 10400, Thailand;2.Department of Clinical Tropical Medicine, Faculty of Tropical Medicine, Mahidol University, 420/6, Ratchawithi Road, Ratchathewi, Bangkok, 10400, Thailand;3.Department of Pathology, Faculty of Medicine and Bosch Institute, University of Sydney, 92-94, Parramatta Road, Camperdown, NSW, 2050, Australia |
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Abstract: | The mechanisms leading to cerebral malaria (CM) are not completely understood. Brain edema has been suggested as having an important role in experimental CM. In this study, CBA/CaH mice were infected with Plasmodium berghei ANKA blood-stage and when typical symptoms of CM developed on day 7, brain tissues were processed for electron-microscopic and immunohistochemical studies. The study demonstrated ultrastructural hallmarks of cerebral edema by perivascular edema and astroglial dilatation confirming existing evidence of vasogenic and cytogenic edema. This correlates closely with the clinical features of CM. An adaptive response of astrocytic activity, represented by increasing glial fibrillary acidic protein (GFAP) expression in the perivascular area and increasing numbers of large astrocyte clusters were predominately found in the CM mice. The presence of multivesicular and lamellar bodies indicates the severity of cerebral damage in experimental CM. Congestion of the microvessels with occluded white blood cells (WBCs), parasitized red blood cells (PRBCs) and platelets is also a crucial covariate role for CM pathogenesis. |
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Keywords: | Electron microscope brain edema rodent cerebral malaria glial fibrillary acidic protein (GFAP) |
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