Document Detail

Prior SO2 exposure promotes airway inflammation and subepithelial fibrosis following repeated ovalbumin challenge.
MedLine Citation:
PMID:  18631350     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Exposure to allergens or air pollutants often leads to asthma exacerbations associated with aggravation of airway inflammation. Although, repeated allergen challenge often induces chronic allergic airway inflammation (CAAI) and airway remodelling, yet, the effects of brief exposure to air pollutants such as SO(2) on development of CAAI and airway remodelling remain to be clarified. OBJECTIVE: The aim of the experiment was to investigate the effects of acute neutrophilic airway inflammation induced by brief exposure to SO(2) on development of CAAI and subepithelial fibrosis (SEF) in a murine model of asthma. METHODS: Acute airway inflammation was induced by brief exposure to 50 p.p.m. SO(2) (1 h/d, 3 days). CAAI and SEF in BALB/c mice were induced by repeated challenge with ovalbumin (OVA) for 5 or 9 weeks with or without prior exposure to SO(2). Bronchoalveolar lavage fluid (BALF) eosinophilia as index of CAAI, BALF endothelin-1 (ET-1) and TGF-beta1 levels, morphometric evaluation of fibrotic area beneath subbasement membrane and lung hydroxyproline content (Hyp) as indexes of SEF were monitored. RESULTS: Exposure to SO(2) led to acute neutrophilic inflammation and epithelial sloughing with profound elevation of BALF ET-1. Repeated OVA challenge resulted in CAAI and SEF along with elevation of Hyp, increase of fibrotic area beneath subbasement membrane and elevation of BALF TGF-beta1. Preceding SO(2) exposure exaggerated BALF eosinophilia, facilitated and enhanced SEF with more significant elevation of BALF ET-1 and TGF-beta1 levels compared with OVA-challenged mice without prior exposure to SO(2). The increase of Hyp was positively correlated with elevation of BALF TGF-beta1 during CAAI (r=0.842, P<0.01). CONCLUSION: This data demonstrated that SEF developed in parallel with severity and time course of CAAI following repeated OVA challenge. SO(2)-induced acute epithelial injury and neutrophilic inflammation could enhance CAAI and promote SEF, probably through overexpression of ET-1 and TGF-beta1.
C Cai; J Xu; M Zhang; X-D Chen; L Li; J Wu; H-W Lai; N-S Zhong
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-06-23
Journal Detail:
Title:  Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology     Volume:  38     ISSN:  1365-2222     ISO Abbreviation:  Clin. Exp. Allergy     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-10-30     Completed Date:  2009-01-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8906443     Medline TA:  Clin Exp Allergy     Country:  England    
Other Details:
Languages:  eng     Pagination:  1680-7     Citation Subset:  IM    
Department of Pulmonology, No. 1 Hospital of Beijing University, Beijing, China.
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MeSH Terms
Air Pollutants / immunology,  toxicity*
Allergens / immunology*
Bronchitis / chemically induced*,  immunology*
Bronchoalveolar Lavage Fluid / cytology,  immunology
Chronic Disease
Endothelin-1 / analysis,  immunology
Lung / drug effects,  immunology,  pathology
Mice, Inbred BALB C
Neutrophils / drug effects,  immunology
Ovalbumin / immunology
Pulmonary Fibrosis / chemically induced*,  immunology*
Respiratory Mucosa / drug effects,  immunology,  pathology
Sulfur Dioxide / immunology,  toxicity*
Transforming Growth Factor beta / analysis,  immunology
Reg. No./Substance:
0/Air Pollutants; 0/Allergens; 0/Endothelin-1; 0/Transforming Growth Factor beta; 7446-09-5/Sulfur Dioxide; 9006-59-1/Ovalbumin

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