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Expression of growth factors by airway epithelial cells in a model of chronic asthma: regulation and relationship to subepithelial fibrosis.
Clin Exp Allergy. 2004 Apr; 34(4):567-75.CE

Abstract

BACKGROUND

Growth factors produced by airway epithelial cells may be important in the pathogenesis of subepithelial fibrosis, a distinctive lesion of chronic human asthma.

OBJECTIVE

To examine the relationship between the development of subepithelial fibrosis and the expression of transforming growth factor-beta 1 (TGF-beta 1) and ligands for the epidermal growth factor receptor.

METHODS

BALB/c mice sensitized to ovalbumin were chronically challenged by inhalation of low levels of antigen, leading to development of subepithelial fibrosis and other changes of airway wall remodelling. Growth factor expression was assessed by immunohistochemistry and enzyme immunoassay.

RESULTS

Allergic sensitization directly correlated with airway epithelial expression of both the cleaved, potentially biologically active form of TGF-beta 1 and of amphiregulin in response to allergen challenge. Accumulation of TGF-beta 1 was related to remodelling of the airway wall in chronic asthma, whereas expression of amphiregulin did not exhibit a similar relationship. Production of epithelial cell-derived TGF-beta 1 appeared to be regulated by IL-13, while both IL-13 and CD4(+) T cells regulated accumulation of TGF-beta 1. In contrast to results reported in high-level exposure models of airway fibrosis, eosinophils did not appear to be a significant source of TGF-beta 1.

CONCLUSION

Airway epithelial cell-derived TGF-beta 1 has a potentially crucial role in the development of airway wall remodelling in asthma. Immunological mechanisms may regulate the release and accumulation of TGF-beta 1.

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

15080809

Citation

Kumar, R K., et al. "Expression of Growth Factors By Airway Epithelial Cells in a Model of Chronic Asthma: Regulation and Relationship to Subepithelial Fibrosis." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 34, no. 4, 2004, pp. 567-75.
Kumar RK, Herbert C, Foster PS. Expression of growth factors by airway epithelial cells in a model of chronic asthma: regulation and relationship to subepithelial fibrosis. Clin Exp Allergy. 2004;34(4):567-75.
Kumar, R. K., Herbert, C., & Foster, P. S. (2004). Expression of growth factors by airway epithelial cells in a model of chronic asthma: regulation and relationship to subepithelial fibrosis. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 34(4), 567-75.
Kumar RK, Herbert C, Foster PS. Expression of Growth Factors By Airway Epithelial Cells in a Model of Chronic Asthma: Regulation and Relationship to Subepithelial Fibrosis. Clin Exp Allergy. 2004;34(4):567-75. PubMed PMID: 15080809.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Expression of growth factors by airway epithelial cells in a model of chronic asthma: regulation and relationship to subepithelial fibrosis. AU - Kumar,R K, AU - Herbert,C, AU - Foster,P S, PY - 2004/4/15/pubmed PY - 2004/7/21/medline PY - 2004/4/15/entrez SP - 567 EP - 75 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin Exp Allergy VL - 34 IS - 4 N2 - BACKGROUND: Growth factors produced by airway epithelial cells may be important in the pathogenesis of subepithelial fibrosis, a distinctive lesion of chronic human asthma. OBJECTIVE: To examine the relationship between the development of subepithelial fibrosis and the expression of transforming growth factor-beta 1 (TGF-beta 1) and ligands for the epidermal growth factor receptor. METHODS: BALB/c mice sensitized to ovalbumin were chronically challenged by inhalation of low levels of antigen, leading to development of subepithelial fibrosis and other changes of airway wall remodelling. Growth factor expression was assessed by immunohistochemistry and enzyme immunoassay. RESULTS: Allergic sensitization directly correlated with airway epithelial expression of both the cleaved, potentially biologically active form of TGF-beta 1 and of amphiregulin in response to allergen challenge. Accumulation of TGF-beta 1 was related to remodelling of the airway wall in chronic asthma, whereas expression of amphiregulin did not exhibit a similar relationship. Production of epithelial cell-derived TGF-beta 1 appeared to be regulated by IL-13, while both IL-13 and CD4(+) T cells regulated accumulation of TGF-beta 1. In contrast to results reported in high-level exposure models of airway fibrosis, eosinophils did not appear to be a significant source of TGF-beta 1. CONCLUSION: Airway epithelial cell-derived TGF-beta 1 has a potentially crucial role in the development of airway wall remodelling in asthma. Immunological mechanisms may regulate the release and accumulation of TGF-beta 1. SN - 0954-7894 UR - https://www.unboundmedicine.com/medline/citation/15080809/Expression_of_growth_factors_by_airway_epithelial_cells_in_a_model_of_chronic_asthma:_regulation_and_relationship_to_subepithelial_fibrosis_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0954-7894&date=2004&volume=34&issue=4&spage=567 DB - PRIME DP - Unbound Medicine ER -