Early invasion of brain parenchyma by African trypanosomes.

Human African trypanosomiasis or sleeping sickness is a vector-borne parasitic disease that has a major impact on human health and welfare in sub-Saharan countries. Based mostly on data from animal models, it is currently thought that trypanosome entry into the brain occurs by initial infection of t...

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Autores principales:	Ute Frevert, Alexandru Movila, Olga V Nikolskaia, Jayne Raper, Zachary B Mackey, Maha Abdulla, James McKerrow, Dennis J Grab
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b082d354a1404c02a52d601c38d2b926
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spelling	oai:doaj.org-article:b082d354a1404c02a52d601c38d2b9262021-11-18T07:06:54ZEarly invasion of brain parenchyma by African trypanosomes.1932-620310.1371/journal.pone.0043913https://doaj.org/article/b082d354a1404c02a52d601c38d2b9262012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22952808/?tool=EBIhttps://doaj.org/toc/1932-6203Human African trypanosomiasis or sleeping sickness is a vector-borne parasitic disease that has a major impact on human health and welfare in sub-Saharan countries. Based mostly on data from animal models, it is currently thought that trypanosome entry into the brain occurs by initial infection of the choroid plexus and the circumventricular organs followed days to weeks later by entry into the brain parenchyma. However, Trypanosoma brucei bloodstream forms rapidly cross human brain microvascular endothelial cells in vitro and appear to be able to enter the murine brain without inflicting cerebral injury. Using a murine model and intravital brain imaging, we show that bloodstream forms of T. b. brucei and T. b. rhodesiense enter the brain parenchyma within hours, before a significant level of microvascular inflammation is detectable. Extravascular bloodstream forms were viable as indicated by motility and cell division, and remained detectable for at least 3 days post infection suggesting the potential for parasite survival in the brain parenchyma. Vascular inflammation, as reflected by leukocyte recruitment and emigration from cortical microvessels, became apparent only with increasing parasitemia at later stages of the infection, but was not associated with neurological signs. Extravascular trypanosomes were predominantly associated with postcapillary venules suggesting that early brain infection occurs by parasite passage across the neuroimmunological blood brain barrier. Thus, trypanosomes can invade the murine brain parenchyma during the early stages of the disease before meningoencephalitis is fully established. Whether individual trypanosomes can act alone or require the interaction from a quorum of parasites remains to be shown. The significance of these findings for disease development is now testable.Ute FrevertAlexandru MovilaOlga V NikolskaiaJayne RaperZachary B MackeyMaha AbdullaJames McKerrowDennis J GrabPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 8, p e43913 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ute Frevert Alexandru Movila Olga V Nikolskaia Jayne Raper Zachary B Mackey Maha Abdulla James McKerrow Dennis J Grab Early invasion of brain parenchyma by African trypanosomes.
description	Human African trypanosomiasis or sleeping sickness is a vector-borne parasitic disease that has a major impact on human health and welfare in sub-Saharan countries. Based mostly on data from animal models, it is currently thought that trypanosome entry into the brain occurs by initial infection of the choroid plexus and the circumventricular organs followed days to weeks later by entry into the brain parenchyma. However, Trypanosoma brucei bloodstream forms rapidly cross human brain microvascular endothelial cells in vitro and appear to be able to enter the murine brain without inflicting cerebral injury. Using a murine model and intravital brain imaging, we show that bloodstream forms of T. b. brucei and T. b. rhodesiense enter the brain parenchyma within hours, before a significant level of microvascular inflammation is detectable. Extravascular bloodstream forms were viable as indicated by motility and cell division, and remained detectable for at least 3 days post infection suggesting the potential for parasite survival in the brain parenchyma. Vascular inflammation, as reflected by leukocyte recruitment and emigration from cortical microvessels, became apparent only with increasing parasitemia at later stages of the infection, but was not associated with neurological signs. Extravascular trypanosomes were predominantly associated with postcapillary venules suggesting that early brain infection occurs by parasite passage across the neuroimmunological blood brain barrier. Thus, trypanosomes can invade the murine brain parenchyma during the early stages of the disease before meningoencephalitis is fully established. Whether individual trypanosomes can act alone or require the interaction from a quorum of parasites remains to be shown. The significance of these findings for disease development is now testable.
format	article
author	Ute Frevert Alexandru Movila Olga V Nikolskaia Jayne Raper Zachary B Mackey Maha Abdulla James McKerrow Dennis J Grab
author_facet	Ute Frevert Alexandru Movila Olga V Nikolskaia Jayne Raper Zachary B Mackey Maha Abdulla James McKerrow Dennis J Grab
author_sort	Ute Frevert
title	Early invasion of brain parenchyma by African trypanosomes.
title_short	Early invasion of brain parenchyma by African trypanosomes.
title_full	Early invasion of brain parenchyma by African trypanosomes.
title_fullStr	Early invasion of brain parenchyma by African trypanosomes.
title_full_unstemmed	Early invasion of brain parenchyma by African trypanosomes.
title_sort	early invasion of brain parenchyma by african trypanosomes.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/b082d354a1404c02a52d601c38d2b926
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Early invasion of brain parenchyma by African trypanosomes.

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