El-Assaad Fatima, Combes Valery, Grau Georges Er
Vascular Immunology Unit, Department of Pathology, Sydney Medical School, Medical Foundation Building, The University of Sydney Level 2, Room 20892-94 Parramatta Rd, Sydney, NSW, 2006, Australia.
Professor Chair of Vascular Immunology, Department of Pathology, Sydney Medical School, The University of Sydney, Address: Medical Foundation Building (K25)Room 208, 92 - 94 Parramatta Rd, Sydney, NSW, 2006, Australia.
J Neuroinfect Dis. 2014 Feb;5(1). Epub 2014 Jan 6.
Human cerebral malaria is a severe and often lethal complication of infection. Complex host and parasite interactions should the precise mechanisms involved in the onset of this neuropathology. Adhesion of parasitised red blood cells and host cells to endothelial cells lead to profound endothelial alterations that trigger immunopathological changes, varying degrees of brain oedema and can compromise cerebral blood flow, cause cranial nerve dysfunction and hypoxia. Study of the cerebral pathology in human patients is limited to clinical and genetic field studies in endemic areas, thus cerebral malaria (CM) research relies heavily on experimental models. The availability of malaria models allows study from the inoculation of to the onset of disease and permit invasive experiments. Here, we discuss some aspects of our current understanding of CM, the experimental models available and some important recent findings extrapolated from these models.
人类脑型疟疾是一种严重且往往致命的感染并发症。复杂的宿主与寄生虫相互作用构成了这种神经病理学发病机制的精确过程。被寄生的红细胞和宿主细胞与内皮细胞的黏附会导致内皮细胞发生深刻改变，进而引发免疫病理变化、不同程度的脑水肿，并可能损害脑血流，导致颅神经功能障碍和缺氧。对人类患者脑病理学的研究仅限于流行地区的临床和基因领域研究，因此脑型疟疾（CM）的研究严重依赖实验模型。疟疾模型的可用性使得从接种到疾病发作的整个过程都能得到研究，并且允许进行侵入性实验。在此，我们讨论当前对CM的一些理解、现有的实验模型以及从这些模型中推断出的一些重要近期发现。
