Document Detail


Early immunological response to German cockroach frass exposure induces a Th2/Th17 environment.
MedLine Citation:
PMID:  21051864     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cockroach exposure is a major risk factor for the development of asthma; however, the early immune events induced by cockroach leading to the Th2 response are not fully understood. Exposure of naïve mice to German cockroach (GC) feces (frass) was sufficient to induce dendritic cell (DC) recruiting and activating chemokines C-C motif ligand 20, granulocyte macrophage colony-stimulating factor, granulocyte colony-stimulating factor and macrophage inflammatory protein-1α into the airways. This corresponded with an increase in myeloid DCs (mDCs) in the airways as well as increased expression of CD80 and CD86 on the mDCs. Plasmacytoid DCs in the lung were unchanged. Levels of IL-5, IL-17A and IL-6 cytokines in whole lung cultures were significantly increased 18 h following GC frass exposure demonstrating the early development of a mixed Th2/Th17 response. In addition, GC frass stimulated the production of IL-23, IL-6 and IL-12p70 from bone marrow-derived mDCs. Adoptive transfer of GC frass-pulsed mDCs induced airway reactivity, airway inflammation as well as eosinophilia and induced a strong Th2/Th17 response in the lung. MyD88-deficient bone marrow-derived mDCs did not respond to GC frass treatment, suggesting a functional Toll-like receptor pathway was important to induce the Th2/Th17 response. Together, our data show that GC frass activated the innate immune response to augment DC recruitment and activation of mDCs which promoted robust T cell-skewing cytokines and ultimately drive the development of airway inflammation.
Authors:
Kristen Page; Ping Zhou; John R Ledford; Scottie B Day; Riad Lutfi; Krista Dienger; Ian P Lewkowich
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-11-05
Journal Detail:
Title:  Journal of innate immunity     Volume:  3     ISSN:  1662-8128     ISO Abbreviation:  J Innate Immun     Publication Date:  2011  
Date Detail:
Created Date:  2011-02-22     Completed Date:  2011-06-17     Revised Date:  2012-02-01    
Medline Journal Info:
Nlm Unique ID:  101469471     Medline TA:  J Innate Immun     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  167-79     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 S. Karger AG, Basel.
Affiliation:
Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center and Cincinnati Children's Research Foundation, Ohio 45229, USA. kristen.page@cchmc.org
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MeSH Terms
Descriptor/Qualifier:
Animals
Chemokines / biosynthesis
Cockroaches / immunology*
Cytokines / biosynthesis
Dendritic Cells / immunology
Feces / chemistry*
Female
Immunity, Innate
Lung / cytology,  immunology
Mice
Mice, Inbred BALB C
Pneumonia / immunology
Th17 Cells / immunology*
Th2 Cells / immunology*
Toll-Like Receptors / metabolism
Grant Support
ID/Acronym/Agency:
AR47363/AR/NIAMS NIH HHS; HL075568/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Chemokines; 0/Cytokines; 0/Toll-Like Receptors

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


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