Document Detail


Haemophilus influenzae infection drives IL-17-mediated neutrophilic allergic airways disease.
MedLine Citation:
PMID:  21998577     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A subset of patients with stable asthma has prominent neutrophilic and reduced eosinophilic inflammation, which is associated with attenuated airways hyper-responsiveness (AHR). Haemophilus influenzae has been isolated from the airways of neutrophilic asthmatics; however, the nature of the association between infection and the development of neutrophilic asthma is not understood. Our aim was to investigate the effects of H. influenzae respiratory infection on the development of hallmark features of asthma in a mouse model of allergic airways disease (AAD). BALB/c mice were intraperitoneally sensitized to ovalbumin (OVA) and intranasally challenged with OVA 12-15 days later to induce AAD. Mice were infected with non-typeable H. influenzae during or 10 days after sensitization, and the effects of infection on the development of key features of AAD were assessed on day 16. T-helper 17 cells were enumerated by fluorescent-activated cell sorting and depleted with anti-IL-17 neutralizing antibody. We show that infection in AAD significantly reduced eosinophilic inflammation, OVA-induced IL-5, IL-13 and IFN-γ responses and AHR; however, infection increased airway neutrophil influx in response to OVA challenge. Augmented neutrophilic inflammation correlated with increased IL-17 responses and IL-17 expressing macrophages and neutrophils (early, innate) and T lymphocytes (late, adaptive) in the lung. Significantly, depletion of IL-17 completely abrogated infection-induced neutrophilic inflammation during AAD. In conclusion, H. influenzae infection synergizes with AAD to induce Th17 immune responses that drive the development of neutrophilic and suppress eosinophilic inflammation during AAD. This results in a phenotype that is similar to neutrophilic asthma. Infection-induced neutrophilic inflammation in AAD is mediated by IL-17 responses.
Authors:
Ama-Tawiah Essilfie; Jodie L Simpson; Jay C Horvat; Julie A Preston; Margaret L Dunkley; Paul S Foster; Peter G Gibson; Philip M Hansbro
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-10-06
Journal Detail:
Title:  PLoS pathogens     Volume:  7     ISSN:  1553-7374     ISO Abbreviation:  PLoS Pathog.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-10-14     Completed Date:  2012-02-09     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  101238921     Medline TA:  PLoS Pathog     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e1002244     Citation Subset:  IM    
Affiliation:
Centre for Asthma and Respiratory Diseases and Hunter Medical Research Institute, The University of Newcastle, Newcastle, New South Wales, Australia.
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MeSH Terms
Descriptor/Qualifier:
Animals
Asthma / immunology*,  microbiology,  pathology
Disease Models, Animal
Eosinophils / immunology
Female
Haemophilus Infections / immunology*,  microbiology,  pathology
Haemophilus influenzae / pathogenicity*
Immunity, Cellular
Inflammation / pathology
Interferon-gamma / immunology
Interleukin-13 / immunology
Interleukin-17 / immunology*,  metabolism
Interleukin-5 / immunology
Mice
Mice, Inbred BALB C
Neutrophils / immunology*
Ovalbumin / adverse effects,  immunology
Phenotype
T-Lymphocytes, Regulatory / immunology
Th17 Cells / cytology,  immunology
Chemical
Reg. No./Substance:
0/Interleukin-13; 0/Interleukin-17; 0/Interleukin-5; 82115-62-6/Interferon-gamma; 9006-59-1/Ovalbumin
Comments/Corrections

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


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