Document Detail


IL-27/IFN-γ induce MyD88-dependent steroid-resistant airway hyperresponsiveness by inhibiting glucocorticoid signaling in macrophages.
MedLine Citation:
PMID:  20817868     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Inflammation and airway hyperresponsiveness (AHR) are hallmark features of asthma and often correlate with the severity of clinical disease. Although these features of asthma can be effectively managed with glucocorticoid therapy, a subgroup of patients, typically with severe asthma, remains refractory to therapy. The mechanisms leading to steroid resistance in severe asthmatics are poorly understood but may be related to the activation of innate host defense pathways. Previously, we have shown that IFN-γ-producing cells and LPS, two factors that are associated with severe asthma, induce steroid-resistant AHR in a mouse model. We now demonstrate that cooperative signaling induced by IFN-γ and LPS results in the production of IL-27 by mouse pulmonary macrophages. IL-27 and IFN-γ uniquely cooperate to induce glucocorticoid-resistant AHR through a previously unknown MyD88-dependent mechanism in pulmonary macrophages. Importantly, integrated signaling by IL-27/IFN-γ inhibits glucocorticoid-induced translocation of the glucocorticoid receptor to the nucleus of macrophages. Furthermore, expression of both IL-27 and IFN-γ was increased in the induced sputum of steroid-refractory asthmatics. These results suggest that a potential mechanism for steroid resistance in asthma is the activation of MyD88-dependent pathways in macrophages that are triggered by IL-27 and IFN-γ, and that manipulation of these pathways may be a therapeutic target.
Authors:
Jing Jing Li; Wan Wang; Katherine J Baines; Nikola A Bowden; Philip M Hansbro; Peter G Gibson; Rakesh K Kumar; Paul S Foster; Ming Yang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-03
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-22     Completed Date:  2010-10-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4401-9     Citation Subset:  AIM; IM    
Affiliation:
Centre for Asthma and Respiratory Disease, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia.
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MeSH Terms
Descriptor/Qualifier:
Animals
Asthma / immunology,  metabolism
Bronchial Hyperreactivity / immunology,  metabolism*
Cell Separation
Enzyme-Linked Immunosorbent Assay
Flow Cytometry
Fluorescent Antibody Technique
Glucocorticoids / metabolism*
Humans
Interferon-gamma / immunology,  metabolism*
Interleukins / immunology,  metabolism*
Macrophage Activation / immunology
Macrophages, Alveolar / immunology,  metabolism*
Mice
Mice, Inbred BALB C
Mice, Knockout
Myeloid Differentiation Factor 88 / immunology,  metabolism*
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction / immunology
Chemical
Reg. No./Substance:
0/Glucocorticoids; 0/Il27 protein, mouse; 0/Interleukins; 0/Myd88 protein, mouse; 0/Myeloid Differentiation Factor 88; 82115-62-6/Interferon-gamma

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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