Linked Life Data

20116865

Source:http://linkedlifedata.com/resource/pubmed/id/20116865

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2010-3-9
pubmed:abstractText
Endothelin has been implicated in the pathogenesis of experimental and human Chagas disease. In the present study, we investigated whether the treatment with bosentan, an antagonist of both ET(A)/ET(B) endothelin receptors, modified parasite load and inflammation in the central nervous system (CNS) of Trypanosomacruzi-infected rats. The cerebellum was the most affected region in the CNS with marked parasitism and inflammation. Treatment with bosentan enhanced parasitemia and CNS parasitism, but control of infection was eventually attained. There was also an increase in the levels of the cytokines TNF-alpha, IL-10, IFN-gamma, CCL2/MCP-1, CCL3/MIP-1alpha and CCL5/RANTES in the brain of infected animals at days 9, 13 and 18 after infection. Overall, bosentan has some effects on the expression of certain cytokines and this may be related to the initial enhanced parasite load. Altogether, our data suggest that endothelin action via ET(A) and ET(B) receptors may play a role in the initial resistance of the CNS to T. cruzi infection in rats.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1872-8421
pubmed:author
pubmed:copyrightInfo
Copyright 2010 Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
30
pubmed:volume
220
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
64-8
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Role of endothelin receptors in the control of central nervous system parasitism in Trypanosoma cruzi infection in rats.
pubmed:affiliation
Departamento de Patologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, 31270901, Belo Horizonte, MG, Brazil. milenerachid@ig.com.br
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural