Linked Life Data

17675520

Source:http://linkedlifedata.com/resource/pubmed/id/17675520

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-8-6
pubmed:abstractText
The blood-brain barrier (BBB), which constitutes the interface between blood and cerebral parenchyma, has been shown to be disrupted during retroviral associated neuromyelopathies. Human T cell leukemia virus (HTLV-1)-associated myelopathy/tropical spastic paraparesis is a slowly progressive neurodegenerative disease, in which evidence of BBB breakdown has been demonstrated by the presence of lymphocytic infiltrates in the CNS and plasma protein leakage through cerebral endothelium. Using an in vitro human BBB model, we investigated the cellular and molecular mechanisms involved in endothelial changes induced by HTLV-1-infected lymphocytes. We demonstrate that coculture with infected lymphocytes induces an increase in paracellular endothelial permeability and transcellular migration, via IL-1alpha and TNF-alpha secretion. This disruption is associated with tight junction disorganization between endothelial cells, and alterations in the expression pattern of tight junction proteins such as zonula occludens 1. These changes could be prevented by inhibition of the NF-kappaB pathway or of myosin light chain kinase activity. Such disorganization was confirmed in histological sections of spinal cord from an HTLV-1-associated myelopathy/tropical spastic paraparesis patient. Based on this BBB model, the present data indicate that HTLV-1-infected lymphocytes can induce BBB breakdown and may be responsible for the CNS infiltration that occurs in the early steps of retroviral-associated neuromyelopathies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2576-83
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17675520-Blood-Brain Barrier, pubmed-meshheading:17675520-Cell Line, Transformed, pubmed-meshheading:17675520-Cerebellum, pubmed-meshheading:17675520-Endothelial Cells, pubmed-meshheading:17675520-Endothelium, Vascular, pubmed-meshheading:17675520-Human T-lymphotropic virus 1, pubmed-meshheading:17675520-Humans, pubmed-meshheading:17675520-Interleukin-1alpha, pubmed-meshheading:17675520-Lymphocytes, pubmed-meshheading:17675520-Membrane Proteins, pubmed-meshheading:17675520-Models, Immunological, pubmed-meshheading:17675520-Myosin-Light-Chain Kinase, pubmed-meshheading:17675520-Neurodegenerative Diseases, pubmed-meshheading:17675520-Paraparesis, Tropical Spastic, pubmed-meshheading:17675520-Phosphoproteins, pubmed-meshheading:17675520-Spinal Cord, pubmed-meshheading:17675520-Tight Junctions, pubmed-meshheading:17675520-Tumor Necrosis Factor-alpha
pubmed:year
2007
pubmed:articleTitle
Human blood-brain barrier disruption by retroviral-infected lymphocytes: role of myosin light chain kinase in endothelial tight-junction disorganization.
pubmed:affiliation
Unité d'Epidémiologie et Physiopathologie des Virus Oncogènes, Département de Virologie and Centre National de la Recherche Scientifique Unité de Recherche Associée 3015, Institut Pasteur, Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't