Document Detail


IL-33 exacerbates eosinophil-mediated airway inflammation.
MedLine Citation:
PMID:  20693421     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Bartosz Stolarski; Mariola Kurowska-Stolarska; Peter Kewin; Damo Xu; Foo Y Liew
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-06
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-03     Completed Date:  2010-11-23     Revised Date:  2014-02-19    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3472-80     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
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:
G0801198//Medical Research Council; //Medical Research Council; //Wellcome Trust
Chemical
Reg. No./Substance:
0/Il1rl1 protein, mouse; 0/Inflammation Mediators; 0/Interleukins; 0/Receptors, Interleukin; 0/interleukin-33, mouse

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