Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1996-2-6
pubmed:abstractText
We analyzed the biological role of nitric oxide (NO) during murine Trypanosoma cruzi infection. Infection of mice with T. cruzi markedly increased NO synthesis. Administration of N-nitro-L-arginine methyl-esther (L-NAME) intraperitoneally or intragastrically diminished endogenous NO synthesis and resistance of mice to acute infection with three biologically different strains of T. cruzi. Mice protected against challenge with T. cruzi by transfer of T-cell-enriched populations from chronically infected animals, showed higher serum nitrate levels than controls non-transferred, or transferred, with T cells from non-immune mice. Administration of L-NAME abrogated transfer of resistance, suggesting NO participation in this process. Depletion of T cells from the transferred population abolished both protection and NO3- increase. On the contrary, mice chronically infected with T. cruzi showed no increased parasitemia or death upon treatment with L-NAME. The NO donor drug S-nitroso-acetyl-penicillamine was able to kill tissue culture or bloodstream trypomastigotes in vitro at biologically relevant concentrations. Conversely, NO appeared not to play a role in formation of inflammatory foci during T. cruzi infection, since infected mice treated with L-NAME showed no reduced inflammation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0165-2478
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
121-6
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:articleTitle
Role of nitric oxide in resistance and histopathology during experimental infection with Trypanosoma cruzi.
pubmed:affiliation
Laboratorio de Virología, Hospital de Niños Dr. R. Gutierrez, Buenos Aires, Argentina.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't