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Reversibility of airway inflammation and remodelling following cessation of antigenic challenge in a model of chronic asthma.
Clin Exp Allergy. 2004 Nov; 34(11):1796-802.CE

Abstract

BACKGROUND

Asthma is associated with recruitment of eosinophils, accumulation of chronic inflammatory cells in the airway walls, subepithelial fibrosis and other structural changes of airway wall remodelling. The role of ongoing exposure to allergens in their pathogenesis remains unclear.

OBJECTIVE

To examine whether changes of inflammation and remodelling were reversible following cessation of antigenic challenge in a mouse model of chronic asthma.

METHODS

BALB/c mice sensitized to ovalbumin (OVA) were chronically challenged by inhalation of a low mass concentration of antigen for 8 weeks, leading to development of acute-on-chronic airway inflammation, subepithelial fibrosis and other changes of airway wall remodelling. Epithelial injury was assessed by immunohistochemistry, while inflammation and remodelling were quantified by appropriate histomorphometric techniques. Regression of lesions was assessed in animals examined at 1, 2 and 4 weeks after exposure to OVA ceased.

RESULTS

We did not find evidence of airway epithelial injury in this model of low-level chronic inhalational exposure to antigen. Persistence of the recruitment of eosinophils and chronic inflammatory cells in the airway walls was dependent on continuing antigenic challenge, as was persistence of mucous cell hyperplasia/metaplasia. Subepithelial fibrosis and epithelial hypertrophy exhibited delayed reversibility following cessation of exposure to antigen, possibly related to matrix-associated accumulation of transforming growth factor-beta(1).

CONCLUSION

In chronic asthma, low-level antigenic challenge may be required to maintain the inflammatory response in the airway wall, but airway remodelling may persist in its absence.

Authors+Show Affiliations

Department of Pathology, University of New South Wales, Sydney, Australia. R.Kumar@unsw.edu.auNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15544607

Citation

Kumar, R K., et al. "Reversibility of Airway Inflammation and Remodelling Following Cessation of Antigenic Challenge in a Model of Chronic Asthma." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 34, no. 11, 2004, pp. 1796-802.
Kumar RK, Herbert C, Kasper M. Reversibility of airway inflammation and remodelling following cessation of antigenic challenge in a model of chronic asthma. Clin Exp Allergy. 2004;34(11):1796-802.
Kumar, R. K., Herbert, C., & Kasper, M. (2004). Reversibility of airway inflammation and remodelling following cessation of antigenic challenge in a model of chronic asthma. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 34(11), 1796-802.
Kumar RK, Herbert C, Kasper M. Reversibility of Airway Inflammation and Remodelling Following Cessation of Antigenic Challenge in a Model of Chronic Asthma. Clin Exp Allergy. 2004;34(11):1796-802. PubMed PMID: 15544607.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reversibility of airway inflammation and remodelling following cessation of antigenic challenge in a model of chronic asthma. AU - Kumar,R K, AU - Herbert,C, AU - Kasper,M, PY - 2004/11/17/pubmed PY - 2005/4/14/medline PY - 2004/11/17/entrez SP - 1796 EP - 802 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin Exp Allergy VL - 34 IS - 11 N2 - BACKGROUND: Asthma is associated with recruitment of eosinophils, accumulation of chronic inflammatory cells in the airway walls, subepithelial fibrosis and other structural changes of airway wall remodelling. The role of ongoing exposure to allergens in their pathogenesis remains unclear. OBJECTIVE: To examine whether changes of inflammation and remodelling were reversible following cessation of antigenic challenge in a mouse model of chronic asthma. METHODS: BALB/c mice sensitized to ovalbumin (OVA) were chronically challenged by inhalation of a low mass concentration of antigen for 8 weeks, leading to development of acute-on-chronic airway inflammation, subepithelial fibrosis and other changes of airway wall remodelling. Epithelial injury was assessed by immunohistochemistry, while inflammation and remodelling were quantified by appropriate histomorphometric techniques. Regression of lesions was assessed in animals examined at 1, 2 and 4 weeks after exposure to OVA ceased. RESULTS: We did not find evidence of airway epithelial injury in this model of low-level chronic inhalational exposure to antigen. Persistence of the recruitment of eosinophils and chronic inflammatory cells in the airway walls was dependent on continuing antigenic challenge, as was persistence of mucous cell hyperplasia/metaplasia. Subepithelial fibrosis and epithelial hypertrophy exhibited delayed reversibility following cessation of exposure to antigen, possibly related to matrix-associated accumulation of transforming growth factor-beta(1). CONCLUSION: In chronic asthma, low-level antigenic challenge may be required to maintain the inflammatory response in the airway wall, but airway remodelling may persist in its absence. SN - 0954-7894 UR - https://www.unboundmedicine.com/medline/citation/15544607/Reversibility_of_airway_inflammation_and_remodelling_following_cessation_of_antigenic_challenge_in_a_model_of_chronic_asthma_ DB - PRIME DP - Unbound Medicine ER -