Mechanism and treatment of airway remodeling

Chih His Kuo, Te Chih Hsiung, Chien Da Huang, Han Pin Kuo

Research output: Contribution to journalArticle

Abstract

Airway remodeling is a consequence of asthmatic airway inflammation characterized by submucosal gland hyperplasia, subepithelial fibrosis, extracellular matrix deposition, smooth muscle hypertrophy and submucosal angiogenesis. The remodeled asthmatic airway contributes to the irreversible flow obstruction and bronchial hyper-responsiveness. Activated fibroblasts and myofibrolasts alter the balance of MMP-9 (matrix metalloproteinase -9) and TIMP-1 (tissue inhibitor of matrix metalloproteinase-1) through the stimulation of TGF-beta1 (transforming growth factor-beta1), therefore, promotes the extracellular matrix deposition. Bone marrow derived fibrocytes migrate to the asthmatic airway from blood circulation acts as a progenitor cell of fibroblast and myofibrolast. Chemokines and cytokines implicated in the fibrocytes recruitment orchestrate the complex network of asthmatic inflammation, thereafter, strengthen the asthmatic airway remodeling. Airway smooth muscle which is traditionally known to be a controller of the airway tone, also exhibits phenotype alteration during asthmatic inflammation, and mediates the progression of airway remodeling. Based on the finding that severity of airway remodeling sometimes disproportionate to the history of asthma, a new insight of the asthma points out the parallel contribution of airway remodeling and asthmatic inflammation. Currently, inhaled corticosteroid is the standard treatment of asthma, and the early administration of inhaled corticosteroid is the most effective strategy to prevent airway remodeling. Hydrofluoroalkane (HFA)-ciclesonide, a newer inhaled corticosteroid with fine particles which exhibits good lung deposition, effectively suppresses the asthmatic small airway inflammation. Leukotriene C4 and D4 which are recently known to mediate the fibroblast proliferation and extracellular matrix deposition, poses leukotriene antagonist a reasonable choice for further investigation of airway remodeling therapy. Furthermore, based on the finding of murine asthmatic models, epidermal growth factor receptor tyrosine kinase and vascular endothelial growth factor are the future therapeutic targets of asthmatic airway remodeling.

Original languageEnglish
Pages (from-to)129-138
Number of pages10
JournalJournal of Internal Medicine of Taiwan
Volume20
Issue number2
Publication statusPublished - Apr 1 2009
Externally publishedYes

Fingerprint

Airway Remodeling
Inflammation
Extracellular Matrix
Adrenal Cortex Hormones
HFA 134a
Asthma
Fibroblasts
Smooth Muscle
Leukotriene D4
Leukotriene Antagonists
Transforming Growth Factor beta1
Leukotriene C4
Matrix Metalloproteinase 1
Tissue Inhibitor of Metalloproteinase-1
Matrix Metalloproteinase Inhibitors
Blood Circulation
Matrix Metalloproteinase 9
Chemokines
Epidermal Growth Factor Receptor
Protein-Tyrosine Kinases

Keywords

  • Airway remodeling
  • Airway smooth muscle
  • Asthma
  • Fibrocyte
  • Inhaled corticosteroid

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Kuo, C. H., Hsiung, T. C., Huang, C. D., & Kuo, H. P. (2009). Mechanism and treatment of airway remodeling. Journal of Internal Medicine of Taiwan, 20(2), 129-138.

Mechanism and treatment of airway remodeling. / Kuo, Chih His; Hsiung, Te Chih; Huang, Chien Da; Kuo, Han Pin.

In: Journal of Internal Medicine of Taiwan, Vol. 20, No. 2, 01.04.2009, p. 129-138.

Research output: Contribution to journalArticle

Kuo, CH, Hsiung, TC, Huang, CD & Kuo, HP 2009, 'Mechanism and treatment of airway remodeling', Journal of Internal Medicine of Taiwan, vol. 20, no. 2, pp. 129-138.
Kuo, Chih His ; Hsiung, Te Chih ; Huang, Chien Da ; Kuo, Han Pin. / Mechanism and treatment of airway remodeling. In: Journal of Internal Medicine of Taiwan. 2009 ; Vol. 20, No. 2. pp. 129-138.
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