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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2008-12-16
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pubmed:abstractText |
Differentiating between injurious and reparative factors facilitates appropriate therapeutic intervention. We evaluated the role of tumor necrosis factor alpha (TNFalpha) in parenchymal brain pathology resolution following virus-induced encephalitis from a picornavirus, Theiler's murine encephalomyelitis virus (TMEV). We infected the following animals with TMEV for 7 to 270 days: B6/129 TNF(-/-) mice (without TNFalpha expression), B6/129 TNFR1(-/-) mice (without TNFalpha receptor 1 expression), and B6/129 TNFR2(-/-) mice (without TNFalpha receptor 2 expression). Normal TNFalpha-expressing controls were TMEV-infected B6, 129/J, B6/129F1 and B6/129F2 mice. Whereas all strains developed inflammation and neuronal injury in the hippocampus and striatum 7 to 21 days postinfection (dpi), the control mice resolved the pathology by 45 to 90 dpi. However, parenchymal hippocampal and striatal injury persisted in B6/129 TNF(-/-) mice following infection. Treating virus-infected mice with active recombinant mouse TNFalpha resulted in less hippocampal and striatal pathology, whereas TNFalpha-neutralizing treatment worsened pathology. T1 "black holes" appeared on MRI during early infection in the hippocampus and striatum in all mice but persisted only in TNF(-/-) mice. TNFR2 [corrected] mediated hippocampal pathology resolution whereas TNFR1 [corrected] mediated striatal healing. These findings indicate the role of TNFalpha in resolution of sublethal hippocampal and striatal injury.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-10378869,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-10411942,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-10841576,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-10936200,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-11391700,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-11549714,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-11600888,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-11917000,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-12440382,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-12938226,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-14977539,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-14999074,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-15155767,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-16337385,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-164412,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-2279004,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-2407753,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-7561103,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-7600284,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-7880718,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-8525642,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-8673925,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-8960740,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-9222347,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-9348316,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-9736029,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18422761-9989447
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1750-3639
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
19
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
12-26
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pubmed:dateRevised |
2011-8-4
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pubmed:meshHeading |
pubmed-meshheading:18422761-Analysis of Variance,
pubmed-meshheading:18422761-Animals,
pubmed-meshheading:18422761-Brain,
pubmed-meshheading:18422761-Corpus Striatum,
pubmed-meshheading:18422761-Encephalitis,
pubmed-meshheading:18422761-Hippocampus,
pubmed-meshheading:18422761-Host-Pathogen Interactions,
pubmed-meshheading:18422761-Immunohistochemistry,
pubmed-meshheading:18422761-Magnetic Resonance Imaging,
pubmed-meshheading:18422761-Mice,
pubmed-meshheading:18422761-Mice, Inbred Strains,
pubmed-meshheading:18422761-Mice, Knockout,
pubmed-meshheading:18422761-Neurons,
pubmed-meshheading:18422761-Receptors, Tumor Necrosis Factor, Type I,
pubmed-meshheading:18422761-Receptors, Tumor Necrosis Factor, Type II,
pubmed-meshheading:18422761-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:18422761-Spinal Cord,
pubmed-meshheading:18422761-Theilovirus,
pubmed-meshheading:18422761-Tumor Necrosis Factor-alpha
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pubmed:year |
2009
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pubmed:articleTitle |
Tumor necrosis factor alpha is reparative via TNFR2 [corrected] in the hippocampus and via TNFR1 [corrected] in the striatum after virus-induced encephalitis.
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pubmed:affiliation |
Department of Immunology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. rodriguez.moses@mayo.edu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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