Source:http://linkedlifedata.com/resource/pubmed/id/11919547
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2002-3-28
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| pubmed:abstractText |
Biocompatibility of implanted materials is determined by the host foreign-body response, which is comprised of cellular (adherent monocytes and macrophages) and soluble (secreted cytokines) components. Modulating the presence, activity or both of adherent macrophages may increase or decrease the biocompatibility of implants because these cells remain adherent to the implant surface and fuse to form foreign-body giant cells (FBGCs), leading to failure of the implant. An attractive mechanism of eliminating these cells is through the induction of apoptosis; therefore ways of inducing or inhibiting apoptosis of biomaterial-adherent inflammatory cells are being investigated. We hypothesized that interleukin-4 (IL-4) promotes macrophage survival by inhibiting tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis. We found that TNF-alpha induces apoptosis in a time- and dose-dependent manner, whereas IL-4 inhibits TNF-alpha-induced and spontaneous apoptosis of biomaterial-adherent macrophages. Blocking experiments and evaluation of shedding of soluble TNF receptor type I (TNF-RI) demonstrated that endogenous TNF-alpha production is responsible for spontaneous apoptosis of biomaterial-adherent cells and that IL-4 inhibits this apoptosis by increasing levels of shedding of soluble TNF-RI. These findings suggest that TNF-alpha and IL-4 play key roles in determining the fate of biomaterial-adherent cells and that fusion of macrophages into FBGCs is a mechanism for promoting inflammatory-cell survival on implanted materials.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Biocompatible Materials,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0022-2143
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
139
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
90-100
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:11919547-Adult,
pubmed-meshheading:11919547-Antigens, CD,
pubmed-meshheading:11919547-Apoptosis,
pubmed-meshheading:11919547-Biocompatible Materials,
pubmed-meshheading:11919547-Cell Adhesion,
pubmed-meshheading:11919547-Cell Survival,
pubmed-meshheading:11919547-Cells, Cultured,
pubmed-meshheading:11919547-Drug Interactions,
pubmed-meshheading:11919547-Foreign-Body Reaction,
pubmed-meshheading:11919547-Giant Cells,
pubmed-meshheading:11919547-Humans,
pubmed-meshheading:11919547-In Situ Nick-End Labeling,
pubmed-meshheading:11919547-Interleukin-4,
pubmed-meshheading:11919547-Macrophages,
pubmed-meshheading:11919547-Microscopy, Electron, Scanning,
pubmed-meshheading:11919547-Monocytes,
pubmed-meshheading:11919547-Prostheses and Implants,
pubmed-meshheading:11919547-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:11919547-Receptors, Tumor Necrosis Factor, Type I,
pubmed-meshheading:11919547-Tumor Necrosis Factor-alpha
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| pubmed:year |
2002
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| pubmed:articleTitle |
Interleukin-4 inhibits tumor necrosis factor-alpha-induced and spontaneous apoptosis of biomaterial-adherent macrophages.
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| pubmed:affiliation |
Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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