Linked Life Data

16002713

Source:http://linkedlifedata.com/resource/pubmed/id/16002713

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-7-8
pubmed:abstractText
Distal sensory polyneuropathy (DSP) is currently the most common neurological complication of HIV infection in the developed world and is characterized by sensory neuronal injury accompanied by inflammation, which is clinically manifested as disabling pain and gait instability. We previously showed that feline immunodeficiency virus (FIV) infection of cats caused DSP together with immunosuppression in cats, similar to that observed in HIV-infected humans. In this study, we investigated the pathogenic mechanisms underlying the development of FIV-induced DSP using feline dorsal root ganglia (DRG) cultures, consisting of neurons, Schwann cells, and macrophages. FIV-infected cultures exhibited viral Ags (p24 and envelope) in macrophages accompanied by neuronal injury, indicated by neurite retraction, neuronal loss and decreased soma size, compared with mock-infected (control) cultures. FIV infection up-regulated inducible NO synthase (iNOS), STAT-1, and TNF-alpha mRNA levels in DRG cultures. Increased STAT-1 and iNOS mRNA levels were also observed in DRGs from FIV-infected animals relative to mock-infected controls. Similarly, immunolabeling studies of DRGs from FIV-infected animals showed that macrophages were the principal sources of STAT-1 and iNOS protein production. The iNOS inhibitor aminoguanidine reduced nitrotyrosine and protein carbonyl levels, together with preventing neuronal injury in FIV-infected DRG cultures. The present studies indicate that FIV infection of DRGs directly contributes to axonal and neuronal injury through a mechanism involving macrophage immune activation, which is mediated by STAT-1 and iNOS activation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
175
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1118-26
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16002713-Animals, pubmed-meshheading:16002713-Cats, pubmed-meshheading:16002713-Cells, Cultured, pubmed-meshheading:16002713-DNA-Binding Proteins, pubmed-meshheading:16002713-Enzyme Inhibitors, pubmed-meshheading:16002713-Free Radicals, pubmed-meshheading:16002713-Ganglia, Spinal, pubmed-meshheading:16002713-Guanidines, pubmed-meshheading:16002713-Immunodeficiency Virus, Feline, pubmed-meshheading:16002713-Macrophage Activation, pubmed-meshheading:16002713-Macrophages, pubmed-meshheading:16002713-Neurons, Afferent, pubmed-meshheading:16002713-Nitric Oxide Synthase, pubmed-meshheading:16002713-Nitric Oxide Synthase Type II, pubmed-meshheading:16002713-Organ Culture Techniques, pubmed-meshheading:16002713-Oxidation-Reduction, pubmed-meshheading:16002713-Polyneuropathies, pubmed-meshheading:16002713-STAT1 Transcription Factor, pubmed-meshheading:16002713-Trans-Activators, pubmed-meshheading:16002713-Up-Regulation
pubmed:year
2005
pubmed:articleTitle
Lentivirus infection causes neuroinflammation and neuronal injury in dorsal root ganglia: pathogenic effects of STAT-1 and inducible nitric oxide synthase.
pubmed:affiliation
Department of Clinical Neuroscience, University of Calgary, Calgary, Alberta, Canada.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural