Source:http://linkedlifedata.com/resource/pubmed/id/20055810
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2010-4-26
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pubmed:abstractText |
Epithelial to mesenchymal transition (EMT) has been implicated in the pathogenesis of obliterative bronchiolitis (OB) after lung transplant. Although TNF-alpha accentuates TGF-beta1 driven EMT in primary human bronchial epithelial cells (PBECs), we hypothesized that other acute pro-inflammatory cytokines elevated in the airways of patients with OB may also accentuate EMT and contribute to dysregulated epithelial wound repair. PBECs from lung transplant recipients were stimulated with TGF-beta1+/-IL-1beta, IL-8, TNF-alpha or activated macrophages in co-culture and EMT assessed. The quality and rate of wound closure in a standardized model of lung epithelial injury was assessed in response to above stimuli. Co-treatment with TGF-beta1+TNF-alpha or IL-1beta significantly accentuates phenotypic and some functional features of EMT compared to TGF-beta1 alone. Co-treatment with TGF-beta1+TNF-alpha or IL-1beta accelerates epithelial wound closure however the quality of repair is highly dysregulated. Co-treatment with TGF-beta1+IL-8 has no significant effect on EMT or the speed or quality of wound healing. Activated macrophages dramatically accentuate TGF-beta1-driven EMT and cause dysregulated wound repair. Crosstalk between macrophage-derived acute inflammation in the airway and elevated TGF-beta1 may favor dysregulated airway epithelial repair and fibrosis in the lung allograft via EMT.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1600-6143
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
498-509
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pubmed:meshHeading |
pubmed-meshheading:20055810-Cell Line, Tumor,
pubmed-meshheading:20055810-Coculture Techniques,
pubmed-meshheading:20055810-Epithelium,
pubmed-meshheading:20055810-Fibrosis,
pubmed-meshheading:20055810-Humans,
pubmed-meshheading:20055810-Inflammation,
pubmed-meshheading:20055810-Interleukin-1beta,
pubmed-meshheading:20055810-Interleukin-8,
pubmed-meshheading:20055810-Lung Transplantation,
pubmed-meshheading:20055810-Macrophages,
pubmed-meshheading:20055810-Mesoderm,
pubmed-meshheading:20055810-Models, Biological,
pubmed-meshheading:20055810-Transforming Growth Factor beta1,
pubmed-meshheading:20055810-Tumor Necrosis Factor-alpha,
pubmed-meshheading:20055810-Wound Healing
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pubmed:year |
2010
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pubmed:articleTitle |
Inflammation and epithelial to mesenchymal transition in lung transplant recipients: role in dysregulated epithelial wound repair.
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pubmed:affiliation |
Applied Immunobiology and Transplantation Research Group, Institute of Cellular Medicine, Newcastle University, Newcastle, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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