Source:http://linkedlifedata.com/resource/pubmed/id/16713113
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
2006-7-24
|
pubmed:abstractText |
There are increasing data in support of the hypothesis that inflammatory cytokines are involved in neonatal white matter damage. Despite extensive study of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta, the role of interleukin-6 in the development of white matter damage is largely unknown. In the present study, the role(s) of interleukin-6 in mediating lipopolysaccharide-induced brain injury and behavioral changes was investigated by the intracerebral injection of lipopolysaccharide with interleukin-6 neutralizing antibody in the 5-day-old rat brain. Brain injury was examined in brain sections at postnatal day 8 and postnatal day 21. Behavioral tests including righting reflex, wire hanging maneuver, cliff avoidance, locomotor activity, gait analysis, responses in the elevated plus-maze and passive avoidance were performed from postnatal day 3 to postnatal day 21. Changes in astroglia, microglia and oligodendrocytes were studied using immunohistochemistry in the postnatal day 21 rat brain. Our results show that interleukin-6 antibody attenuated lipopolysaccharide-induced brain lateral ventricle dilation and improved neurobehavioral performance. Interleukin-6 antibody also suppressed lipopolysaccharide-induced astrogliosis and microglial activation, and increased the number of oligodendrocytes in white matter. However, no changes of tumor necrosis factor-alpha and interleukin-1beta were detected. In contrast, no histopathological changes and glial activation were observed in rats injected with only interleukin-6. The present study indicates that the contribution to brain injury by interleukin-6 depends on its interaction with other lipopolysaccharide-induced agents and not on interleukin-6 alone.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0306-4522
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
25
|
pubmed:volume |
141
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
745-55
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:16713113-Age Factors,
pubmed-meshheading:16713113-Animals,
pubmed-meshheading:16713113-Animals, Newborn,
pubmed-meshheading:16713113-Antibodies,
pubmed-meshheading:16713113-Avoidance Learning,
pubmed-meshheading:16713113-Behavior, Animal,
pubmed-meshheading:16713113-Body Weight,
pubmed-meshheading:16713113-Brain Injuries,
pubmed-meshheading:16713113-Cell Count,
pubmed-meshheading:16713113-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:16713113-Female,
pubmed-meshheading:16713113-Immunohistochemistry,
pubmed-meshheading:16713113-Interleukin-1,
pubmed-meshheading:16713113-Interleukin-6,
pubmed-meshheading:16713113-Lipopolysaccharides,
pubmed-meshheading:16713113-Male,
pubmed-meshheading:16713113-Maze Learning,
pubmed-meshheading:16713113-Motor Activity,
pubmed-meshheading:16713113-Psychomotor Performance,
pubmed-meshheading:16713113-Rats,
pubmed-meshheading:16713113-Rats, Sprague-Dawley,
pubmed-meshheading:16713113-Tumor Necrosis Factor-alpha
|
pubmed:year |
2006
|
pubmed:articleTitle |
Role of interleukin-6 in lipopolysaccharide-induced brain injury and behavioral dysfunction in neonatal rats.
|
pubmed:affiliation |
Department of Pediatrics, Division of Newborn Medicine, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA.
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|