Document Detail


IL-33 mediates multi-walled carbon nanotube (MWCNT)-induced airway hyper-reactivity via the mobilization of innate helper cells in the lung.
MedLine Citation:
PMID:  22686327     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Allergic asthma is a chronic inflammatory disorder of the airway associated with bronchial obstruction, airway hyper-reactivity (AHR), and mucus production. The epithelium may direct and propagate asthmatic-like responses. Central to this theory is the observation that viruses, air pollution, and allergens promote epithelial damage and trigger the generation of IL-25, IL-33, and TSLP via innate pathways such as TLRs and purinergic receptors. Similarly, engineered nanomaterials promote a Th2-associated pathophysiology. In this study, we tested the hypothesis that instillation of multi-walled carbon nanotubes (MWCNT) impair pulmonary function in C57Bl/6 mice due to the development of IL-33-dependent Th2-associated inflammation. MWCNT exposure resulted in elevated levels of IL-33 in the lavage fluid (likely originating from airway epithelial cells), enhanced AHR, eosinophil recruitment, and production of Th2-associated cytokines and chemokines. Moreover, these events were dependent on IL-13 signaling and the IL-33/ST2 axis, but independent of T and B cells. Finally, MWCNT exposure resulted in the recruitment of innate lymphoid cells. Collectively, our data suggest that MWCNT induce epithelial damage that results in release of IL-33, which in turn promotes innate lymphoid cell recruitment and the development of IL-13-dependent inflammatory response.
Authors:
Celine A Beamer; Teri A Girtsman; Benjamin P Seaver; Krissy J Finsaas; Christopher T Migliaccio; Victoria K Perry; James B Rottman; Dirk E Smith; Andrij Holian
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-06-29
Journal Detail:
Title:  Nanotoxicology     Volume:  7     ISSN:  1743-5404     ISO Abbreviation:  Nanotoxicology     Publication Date:  2013 Sep 
Date Detail:
Created Date:  2013-08-06     Completed Date:  2014-02-27     Revised Date:  2014-07-06    
Medline Journal Info:
Nlm Unique ID:  101233132     Medline TA:  Nanotoxicology     Country:  England    
Other Details:
Languages:  eng     Pagination:  1070-81     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line
Epithelial Cells / drug effects
Homeodomain Proteins / genetics,  metabolism
Immunity, Innate / drug effects*
Inflammation / metabolism
Interleukin-13 / genetics,  metabolism
Interleukins / genetics,  metabolism*
Lung / cytology*,  drug effects*
Mice
Mice, Inbred C57BL
Mice, Knockout
Nanotubes, Carbon / chemistry,  toxicity*
Pulmonary Alveoli / cytology,  physiology
Respiratory Hypersensitivity / chemically induced*
T-Lymphocytes, Helper-Inducer / physiology
Grant Support
ID/Acronym/Agency:
F32 ES019816/ES/NIEHS NIH HHS; F32 ES019816/ES/NIEHS NIH HHS; P20 RR017670/RR/NCRR NIH HHS; P20 RR017670/RR/NCRR NIH HHS; P30 GM103338/GM/NIGMS NIH HHS; RC2 ES018742/ES/NIEHS NIH HHS; RC2 ES018742/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Homeodomain Proteins; 0/Interleukin-13; 0/Interleukins; 0/Nanotubes, Carbon; 0/interleukin-33, mouse; 128559-51-3/RAG-1 protein
Comments/Corrections

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


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