Document Detail


Influenza enhances caspase-1 in bronchial epithelial cells from asthmatic volunteers and is associated with pathogenesis.
MedLine Citation:
PMID:  23021143     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The leading cause of asthma exacerbation is respiratory viral infection. Innate antiviral defense pathways are altered in the asthmatic epithelium, yet involvement of inflammasome signaling in virus-induced asthma exacerbation is not known.
OBJECTIVE: This study compared influenza-induced activation of inflammasome and innate immune signaling in human bronchial epithelial cells from volunteers with and without asthma and investigated the role of caspase-1 in epithelial cell antiviral defense.
METHODS: Differentiated primary human bronchial epithelial cells from volunteers with and without asthma were infected with influenza A virus. An inflammasome-specific quantitative real-time polymerase chain reaction array was used to compare baseline and influenza-induced gene expression profiles. Cytokine secretion, innate immune gene expression, and viral replication were compared between human bronchial epithelial cells from volunteers with and without asthma. Immunofluorescence microscopy was used to evaluate caspase-1 and PYCARD colocalization. Tracheal epithelial cells from caspase-1-deficient or wild-type mice were infected with influenza and assessed for antiviral gene expression and viral replication.
RESULTS: Human bronchial epithelial cells from asthmatic volunteers had altered influenza-induced expression of inflammasome-related and innate immune signaling components, which correlated with enhanced production of IL-1β, IL-6, and TNF-α. Specifically, influenza-induced caspase-1 expression was enhanced and localization differed in human bronchial epithelial cells from asthmatic volunteers compared to volunteers without asthma. Influenza-infected tracheal epithelial cells from caspase-1-deficient mice had reduced expression of antiviral genes and viral replication.
CONCLUSION: Caspase-1 plays an important role in the airway epithelial cell response to influenza infection, which is enhanced in asthmatic volunteers, and may contribute to the enhanced influenza-related pathogenesis observed in vivo.
Authors:
Rebecca N Bauer; Luisa E Brighton; Loretta Mueller; Zhidan Xiang; Julia E Rager; Rebecca C Fry; David B Peden; Ilona Jaspers
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  The Journal of allergy and clinical immunology     Volume:  130     ISSN:  1097-6825     ISO Abbreviation:  J. Allergy Clin. Immunol.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-01     Completed Date:  2012-12-11     Revised Date:  2014-04-11    
Medline Journal Info:
Nlm Unique ID:  1275002     Medline TA:  J Allergy Clin Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  958-67.e14     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2012 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Asthma / etiology,  immunology*
Bronchi / immunology*
Caspase 1 / analysis,  physiology*
Cells, Cultured
Cytoskeletal Proteins / analysis
Epithelial Cells / immunology
Female
Humans
Immunity, Innate
Influenza, Human / complications*
Interleukin-1beta / biosynthesis
Mice
Mice, Inbred C57BL
Virus Replication
Grant Support
ID/Acronym/Agency:
ES013611/ES/NIEHS NIH HHS; P30 ES010126/ES/NIEHS NIH HHS; R01 ES013611/ES/NIEHS NIH HHS; T32 ES007126/ES/NIEHS NIH HHS; U19 AI077437/AI/NIAID NIH HHS; U19AI077347/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Cytoskeletal Proteins; 0/Interleukin-1beta; 0/Pycard protein, mouse; EC 3.4.22.36/Caspase 1
Comments/Corrections

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