Linked Life Data

6816079

Source:http://linkedlifedata.com/resource/pubmed/id/6816079

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1983-1-19
pubmed:abstractText
Although the involvement of the nervous system in Chagas' disease is well described, the mechanism of the neuronal destruction is unclear. Immunologic, toxic mechanisms and direct invasion have been advocated. Organotypic cultures of spinal cord and dorsal root ganglion derived from Swiss outbred mice were infected with the Brazil strain of Trypanosoma cruzi. Light microscopic and ultrastructural studies were performed at regular intervals. It was found that trypomastigotes were rapidly taken up by glial and other supporting cells. Neurons were rarely parasitized and demyelination was not evident. Loss of several cytoskeletal components was seen. Dendrites were swollen and axons lost their normal filamentous structures but synaptic membranes remained intact. Mitochondrial swelling was evident even in nonparasitized neurons from infected cultures. By 7-10 days of infection the majority of neurons lost their typical morphology and were eventually destroyed by mechanisms other than direct parasite invasion. Organotypic cultures exposed to T. cruzi-conditioned medium exhibited no change in morphology. Since neurons were found only rarely to be parasitized, it is suggested that neuronal destruction is an indirect result of the parasitism of supporting cells such as glial cells and macrophages.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0002-9637
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1090-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Infection of organotypic cultures of spinal cord and dorsal root ganglia with Trypanosoma cruzi.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't