| Diesel exhaust particles override natural injury-limiting pathways in the lung. | |
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MedLine Citation:
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PMID: 20435687 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Induction of effective inflammation in the lung in response to environmental and microbial stimuli is dependent on cooperative signaling between leukocytes and lung tissue cells. We explored how these inflammatory networks are modulated by diesel exhaust particles (DEP) using cocultures of human monocytes with epithelial cells. Cocultures, or monoculture controls, were treated with DEP in the presence or absence of LPS or flagellin. Production of cytokines was explored by Western blotting and ELISA; cell signaling was analyzed by Western blotting. Here, we show that responses of epithelial cells to DEP are amplified by the presence of monocytes. DEP amplified the responses of cellular cocultures to very low doses of TLR agonists. In addition, in the presence of DEP, the responses induced by LPS or flagellin were less amenable to antagonism by the physiological IL-1 antagonist, IL-1ra. This was paralleled by the uncoupling of IL-1 production and release from monocytes, potentially attributable to an ability of DEP to sequester or degrade extracellular ATP. These data describe a model of inflammation where DEP amplifies responses to low concentrations of microbial agonists and alters the nature of the inflammatory milieu induced by TLR agonists. |
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Authors:
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N Chaudhuri; C Paiva; K Donaldson; R Duffin; L C Parker; I Sabroe |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-04-30 |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 299 ISSN: 1522-1504 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-08-02 Completed Date: 2010-08-25 Revised Date: 2011-08-03 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L263-71 Citation Subset: IM |
Affiliation:
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Univ. of Sheffield, United Kingdom. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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metabolism Cell Line Coculture Techniques Cytokines / biosynthesis Flagellin / pharmacology Humans Inflammation / immunology* Interleukin 1 Receptor Antagonist Protein / immunology Interleukin-1 / physiology Interleukin-1beta / biosynthesis Interleukin-8 / biosynthesis Lipopolysaccharides / pharmacology Lung / immunology* Monocytes / immunology Respiratory Mucosa / cytology Signal Transduction / physiology Toll-Like Receptors / agonists Vehicle Emissions / toxicity* |
| Grant Support | |
ID/Acronym/Agency:
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G116/170//Medical Research Council |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/IL8 protein, human; 0/Interleukin 1 Receptor Antagonist Protein; 0/Interleukin-1; 0/Interleukin-1beta; 0/Interleukin-8; 0/Lipopolysaccharides; 0/Toll-Like Receptors; 0/Vehicle Emissions; 12777-81-0/Flagellin; 56-65-5/Adenosine Triphosphate |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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