Linked Life Data

11122355

Source:http://linkedlifedata.com/resource/pubmed/id/11122355

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2001-2-9
pubmed:abstractText
Interleukin-1 (IL-1) mediates symptoms of sickness during the host response to infection. IL-1 exerts its effects via several subtypes of receptors. To assess the role of IL-1 receptor type I (IL-1RI) in the sickness-inducing effects of IL-1, IL-1beta and the cytokine inducer lipopolysaccharide were administered to IL-1RI-deficient mice (IL-1RI-/-). Sickness was assessed by depression of social exploration, anorexia, immobility and body weight loss. IL-1RI-/- mice were resistant to the sickness-inducing effects of IL-1beta administered intraperitoneally (2 microg/mouse) and intracerebroventricularly (2 ng/mouse), but still fully responsive to lipopolysaccharide administered intraperitoneally (2.5 microg/mouse) and intracerebroventricularly (3 ng/mouse). The sensitivity of IL-1RI-/- mice to lipopolysaccharide was not due to a higher brain expression of proinflammatory cytokines other than IL-1, since lipopolysaccharide-induced expression of brain IL-1 beta, tumour necrosis factor-alpha (TNF-alpha) and IL-6 transcripts were identical in IL-1RI-/- and control mice when measured by semiquantitative reverse-transcriptase polymerase chain reaction 1 h after treatment. Blockade of TNF-alpha action in the brain by intracerebroventricular administration of a fragment of the soluble TNF receptor, TNF binding protein (3.6 microg/mouse), attenuated the depressive effects of intraperitoneal injection of lipopolysaccharide (1 microg/mouse) on behaviour in IL-1RI-/- but not in control mice. Since IL-1RI-/- mice were not more sensitive to intracerebroventricularly TNF-alpha (50 ng) than control mice, these results indicate that IL-1RI mediates the sickness effect of IL-1 and that TNF-alpha simply replaces IL-1 when this last cytokine is deficient.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4447-56
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11122355-Animals, pubmed-meshheading:11122355-Brain, pubmed-meshheading:11122355-Exploratory Behavior, pubmed-meshheading:11122355-Gene Expression Regulation, pubmed-meshheading:11122355-Injections, Intraperitoneal, pubmed-meshheading:11122355-Injections, Intraventricular, pubmed-meshheading:11122355-Interleukin-1, pubmed-meshheading:11122355-Interleukin-6, pubmed-meshheading:11122355-Lipopolysaccharides, pubmed-meshheading:11122355-Mice, pubmed-meshheading:11122355-Mice, Inbred C57BL, pubmed-meshheading:11122355-Mice, Inbred Strains, pubmed-meshheading:11122355-Mice, Knockout, pubmed-meshheading:11122355-Receptors, Interleukin-1, pubmed-meshheading:11122355-Receptors, Interleukin-1 Type I, pubmed-meshheading:11122355-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11122355-Social Behavior, pubmed-meshheading:11122355-Tumor Necrosis Factor-alpha
pubmed:year
2000
pubmed:articleTitle
Role of interleukin-1beta and tumour necrosis factor-alpha in lipopolysaccharide-induced sickness behaviour: a study with interleukin-1 type I receptor-deficient mice.
pubmed:affiliation
INRA-INSERM U394, Institut François Magendie, 1 rue Camille Saint-Saëns, 33077 Bordeaux cedex, France; Université Bordeaux I, 33400 Talence, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't