Linked Life Data

19229714

Source:http://linkedlifedata.com/resource/pubmed/id/19229714

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-2-20
pubmed:abstractText
Brain damage in bacterial meningitis is still a major problem. More knowledge about the triggers and mechanisms of neuronal damage in bacterial meningitis is needed to improve outcome in bacterial meningitis. The most common bacterial meningitis pathogen--Streptococcus pneumoniae--causes caspase activation and neuronal apoptosis in the hippocampus via its toxins and extensive inflammatory potential. Nitric oxide (NO)--produced by inducible nitric oxide synthase (iNOS)--is a major inflammatory mediator clearly upregulated in the cerebrospinal fluid during pneumococcal meningitis. However, its effects in bacterial meningitis are still controversial. This article demonstrates that genetic inactivation of iNOS results in a marked reduction of caspase-3-mediated neuronal damage in experimental murine pneumococcal meningitis. Protection of hippocampal neurons in iNOS knockout mice was not due to differences in intrathecal growth of S. pneumoniae and must therefore be attributed to differences of host inflammatory mediators. This indicates that NO plays an important role in hippocampal caspase-3 activation during pneumococcal meningitis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1563-5279
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
119
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
455-9
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Inducible nitric oxide synthase mediates hippocampal caspase-3 activation in pneumococcal meningitis.
pubmed:affiliation
Department of Neurology, Charite University Medicine, Berlin, Germany. johann.braun@charite.de
pubmed:publicationType
Journal Article