期刊
JOURNAL OF NEUROVIROLOGY
卷 14, 期 5, 页码 344-351出版社
SPRINGER
DOI: 10.1080/13550280802282934
关键词
blood-brain barrier; sleeping sickness; trypanosomes
资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI051464] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI1464-01, R01 AI051464] Funding Source: Medline
The neurological complications of human African trypanosomiasis (HAT) in man caused by the unicellular protozoan parasites Trypanosoma brucei gambiense and T. b. rhodesiense are a consequence of the penetration of the blood-brain barrier (BBB) by trypanosomes that enter the central nervous system (CNS). Yet the mechanisms by which African trypanosomes cross the true BBB comprised of brain microvascular endothelial cells (BMECs) remain unclear. Human BBB models used to determine how African trypanosomes initially interact in vitro with the human BBB proper suggest that parasites cross the human BBB in part by generating Ca2+ activation signals in human BMECs through the activity of parasite cysteine proteases. In vivo murine models of HAT have suggested additional mechanisms of BBB traversal by trypanosomes, with recent compelling evidence for the important role of interferon- in facilitating this process. A clear understanding of how trypanosomes enter the CNS is critical for both understanding the neuropathogenesis of HAT and in developing more effective drug therapies for late-stage disease.
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