Open Access System for Information Sharing

Login Library

 

Article
Cited 9 time in webofscience Cited 9 time in scopus
Metadata Downloads

Role of inducible nitric oxide synthase on the development of virus-associated asthma exacerbation which is dependent on Th1 and Th17 cell responses

Title
Role of inducible nitric oxide synthase on the development of virus-associated asthma exacerbation which is dependent on Th1 and Th17 cell responses
Authors
Shin, TSLee, BJTae, YMKim, YSJeon, SGGho, YSChoi, DCKim, YK
POSTECH Authors
Gho, YS
Date Issued
Oct-2010
Publisher
KOREAN SOC MED BIOCHEMISTRY MOLECULAR BIOLOGY
Abstract
Asthma is characterized by airway inflammation induced by immune dysfunction to inhaled antigens. Although respiratory viral infections are the most common cause of asthma exacerbation, immunologic mechanisms underlying virus-associated asthma exacerbation are controversial. Clinical evidence indicates that nitric oxide (NO) levels in exhaled air are increased in exacerbated asthma patients compared to stable patients. Here, we evaluated the immunologic mechanisms and the role of NO synthases (NOSs) in the development of virus-associated asthma exacerbation. A murine model of virus-associated asthma exacerbation was established using intranasal challenge with ovalbumin (OVA) plus dsRNA for 4 weeks in mice sensitized with OVA plus dsRNA. Lung infiltration of inflammatory cells, especially neutrophils, was increased by repeated challenge with OVA plus dsRNA, as compared to OVA alone. The neutrophilic inflammation enhanced by dsRNA was partly abolished in the absence of IFN-gamma or IL-17 gene expression, whereas unaffected in the absence of IL-13. In terms of the roles of NOSs, dsRNA-enhanced neutrophilic inflammation was significantly decreased in inducible NOS (iNOS)-deficient mice compared to wild type controls
in addition, this phenotype was inhibited by treatment with a non-specific NOS inhibitor (L-NAME) or an specific inhibitor (1400 W), but not with a specific endothelial NOS inhibitor (AP-CAV peptide). Taken together, these findings suggest that iNOS pathway is important in the development of virus-associated exacerbation of neutrophilic inflammation, which is dependent on both Th1 and Th17 cell responses.
URI
http://oasis.postech.ac.kr/handle/2014.oak/25305
DOI
10.3858/EMM.2010.42.10.072
ISSN
1226-3613
Article Type
Article
Citation
EXPERIMENTAL AND MOLECULAR MEDICINE, vol. 42, no. 10, page. 721 - 730, 2010-10
Files in This Item:

qr_code

  • mendeley

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Related Researcher

Researcher

 GHO, YONG SONG
Dept of Life Sciences
Read more

Views & Downloads

Browse