| IL-33 exacerbates eosinophil-mediated airway inflammation. | |
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MedLine Citation:
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PMID: 20693421 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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IL-33 has emerged as an important mediator in the immunopathogenesis of allergy and asthma. However, the role of IL-33 in eosinophil-mediated inflammation has not been fully explored. In this article, we report that IL-33 directly stimulates eosinophil differentiation from CD117(+) progenitors in an IL-5-dependent manner. Although resting eosinophils expressed moderate levels of the IL-33R alpha-chain (ST2L), eosinophils that accumulated in the airways of mice with OVA-induced asthma expressed increased amounts of ST2L. In vitro, IL-33 and GM-CSF are potent inducers of ST2L expression on eosinophils, and IL-33 induced the production of IL-13, CCL17, and TGF-beta by eosinophils. In adoptive-transfer experiments, IL-33 exacerbated eosinophil-mediated airway inflammation by increasing the levels of eosinophils, macrophages, lymphocytes, IL-13, TGF-beta, CCL3, CCL17, and CCL24 in the lungs. IL-33 also enhanced the eosinophil-mediated differentiation of airway macrophages toward the alternatively activated macrophage phenotype in an IL-13-dependent manner. Taken together, this study demonstrates that the IL-33/ST2 signaling pathway activates airway eosinophils that exacerbate airway inflammation in an autocrine and paracrine manner. |
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Authors:
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Bartosz Stolarski; Mariola Kurowska-Stolarska; Peter Kewin; Damo Xu; Foo Y Liew |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-08-06 |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 185 ISSN: 1550-6606 ISO Abbreviation: J. Immunol. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-03 Completed Date: 2010-11-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 3472-80 Citation Subset: AIM; IM |
Affiliation:
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Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, United Kingdom. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Autocrine Communication / genetics, immunology Cell Differentiation / genetics, immunology Cell Proliferation Cells, Cultured Coculture Techniques Eosinophils / immunology*, metabolism, pathology* Hematopoietic Stem Cells / immunology, pathology Humans Inflammation Mediators / adverse effects*, physiology* Interleukins / adverse effects*, physiology* Lung / immunology*, metabolism, pathology* Lymphocyte Subsets / immunology, pathology Macrophages / immunology, pathology Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Paracrine Communication / genetics, immunology Receptors, Interleukin / deficiency, genetics, physiology Signal Transduction / genetics, immunology |
| Grant Support | |
ID/Acronym/Agency:
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//Medical Research Council; //Wellcome Trust |
| Chemical | |
Reg. No./Substance:
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0/Il1rl1 protein, mouse; 0/Inflammation Mediators; 0/Interleukins; 0/Receptors, Interleukin; 0/interleukin-33, mouse |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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