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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
1997-11-7
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pubmed:abstractText |
Treatment of primary monocytes with soluble HIV-Tat protein is associated with increased monocyte metalloproteinase-9 (MMP-9) expression and enhanced beta 2 integrin expression that increases monocyte/endothelial adhesion. These alterations require greater than 12 h of HIV-Tat treatment, suggesting the involvement of intermediate factors. Thus, we have examined the role of cytokines in the HIV-Tat-induced alteration of monocyte function. Treatment of monocytes with HIV-Tat rapidly up-regulated the production of IL-1 beta, IL-6, IL-8, and TNF-alpha, but not IL-3, granulocyte-macrophage CSF, basic fibroblast growth factor, or macrophage-inflammatory protein-1 alpha, and was associated with up-regulation of the corresponding cytokine mRNA. Inclusion of neutralizing anti-cytokine Abs to IL-1 beta or TNF-alpha during the HIV-Tat pretreatment period significantly inhibited the HIV-Tat-induced increase in MMP-9 production, monocyte/endothelial adhesion, and monocyte-dependent endothelial damage. In contrast, neutralizing Abs against IL-6 and IL-8 had no effect. The effects of HIV-Tat treatment, namely MMP-9 production, enhanced monocyte/endothelial cell adhesion, and monocyte-dependent endothelial damage, were mimicked by treating the monocytes with IL-1 beta or TNF-alpha, but not with IL-6 or IL-8. Therefore, the mechanism by which HIV-Tat activates monocyte function is dependent on HIV-Tat-induced production of cytokines (IL-1 beta and TNF-alpha).
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Collagenases,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, tat,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 9,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/tat Gene Products, Human...
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
159
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4077-83
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:9378998-Cell Adhesion,
pubmed-meshheading:9378998-Cells, Cultured,
pubmed-meshheading:9378998-Chemotaxis, Leukocyte,
pubmed-meshheading:9378998-Collagenases,
pubmed-meshheading:9378998-Cytokines,
pubmed-meshheading:9378998-Endothelium, Vascular,
pubmed-meshheading:9378998-Gene Products, tat,
pubmed-meshheading:9378998-HIV-1,
pubmed-meshheading:9378998-Humans,
pubmed-meshheading:9378998-Macrophage Activation,
pubmed-meshheading:9378998-Matrix Metalloproteinase 9,
pubmed-meshheading:9378998-Monocytes,
pubmed-meshheading:9378998-RNA, Messenger,
pubmed-meshheading:9378998-tat Gene Products, Human Immunodeficiency Virus
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pubmed:year |
1997
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pubmed:articleTitle |
Activation of monocytes by HIV-Tat treatment is mediated by cytokine expression.
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pubmed:affiliation |
Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article
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