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Prior SO2 exposure promotes airway inflammation and subepithelial fibrosis following repeated ovalbumin challenge.
Clin Exp Allergy. 2008 Oct; 38(10):1680-7.CE

Abstract

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.

Authors+Show Affiliations

Department of Pulmonology, No. 1 Hospital of Beijing University, Beijing, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18631350

Citation

Cai, C, et al. "Prior SO2 Exposure Promotes Airway Inflammation and Subepithelial Fibrosis Following Repeated Ovalbumin Challenge." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 38, no. 10, 2008, pp. 1680-7.
Cai C, Xu J, Zhang M, et al. Prior SO2 exposure promotes airway inflammation and subepithelial fibrosis following repeated ovalbumin challenge. Clin Exp Allergy. 2008;38(10):1680-7.
Cai, C., Xu, J., Zhang, M., Chen, X. D., Li, L., Wu, J., Lai, H. W., & Zhong, N. S. (2008). Prior SO2 exposure promotes airway inflammation and subepithelial fibrosis following repeated ovalbumin challenge. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 38(10), 1680-7. https://doi.org/10.1111/j.1365-2222.2008.03053.x
Cai C, et al. Prior SO2 Exposure Promotes Airway Inflammation and Subepithelial Fibrosis Following Repeated Ovalbumin Challenge. Clin Exp Allergy. 2008;38(10):1680-7. PubMed PMID: 18631350.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prior SO2 exposure promotes airway inflammation and subepithelial fibrosis following repeated ovalbumin challenge. AU - Cai,C, AU - Xu,J, AU - Zhang,M, AU - Chen,X-D, AU - Li,L, AU - Wu,J, AU - Lai,H-W, AU - Zhong,N-S, Y1 - 2008/06/23/ PY - 2008/7/18/pubmed PY - 2009/1/23/medline PY - 2008/7/18/entrez SP - 1680 EP - 7 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin Exp Allergy VL - 38 IS - 10 N2 - 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. SN - 1365-2222 UR - https://www.unboundmedicine.com/medline/citation/18631350/Prior_SO2_exposure_promotes_airway_inflammation_and_subepithelial_fibrosis_following_repeated_ovalbumin_challenge_ L2 - https://doi.org/10.1111/j.1365-2222.2008.03053.x DB - PRIME DP - Unbound Medicine ER -