Proliferation is not increased in airway myofibroblasts isolated from asthmatics

J. E. Ward, T. Harris, T. Bamford, A. Mast, M. C.F. Pain, C. Robertson, D. Smallwood, T. Tran, J. Wilson, A. G. Stewart

Research output: Contribution to journalArticleResearchpeer-review

41 Citations (Scopus)

Abstract

Airway mesenchymal cells, such as myofibroblasts and airway smooth muscle cells, contribute to inflammation, airway remodelling and hyperresponsiveness in asthma by excessive proliferation and inflammatory mediator production. Using endobronchial biopsies obtained from both nonasthmatic and asthmatic subjects, in situ proliferation was assessed by immunostaining for cyclin D1. The number of immunoreactive cells increased with asthma severity and was restricted to the epithelium and subepithelial connective tissue. Despite increases in smooth muscle area, cyclin D1 was not detected in cells in intact muscle bundles. Biopsy-derived cell cultures were characterised as predominantly myofibroblasts, and were assessed to determine whether proliferation and cytokine production varied with asthma status. Cell enumeration showed that basal proliferation was similar in cells from nonasthmatics and asthmatics, and mitogenic responses to fibroblast growth factor-2, thrombin or serum were either reduced or unchanged in cells from asthmatics. Interleukin (IL)-1-dependent granulocyte-macrophage colony-stimulating factor and IL-8 release was increased in cell supernatants from asthmatics. Thus, increased rates of cellular proliferation identified in situ in the asthmatic airway occurred outside the expanded smooth muscle compartment. Although reduced proliferative responses were observed in cultured myofibroblasts from asthmatics, the increased cytokine production by these cells suggests that this contributes to and may perpetuate ongoing inflammation in asthma. Copyright

Original languageEnglish
Pages (from-to)362-371
Number of pages10
JournalEuropean Respiratory Journal
Volume32
Issue number2
DOIs
Publication statusPublished - Aug 2008

Keywords

  • Airway smooth muscle
  • Asthma
  • Fluticasone propionate
  • Myofibroblast
  • Proliferation
  • Salmeterol

Cite this

Ward, J. E., Harris, T., Bamford, T., Mast, A., Pain, M. C. F., Robertson, C., ... Stewart, A. G. (2008). Proliferation is not increased in airway myofibroblasts isolated from asthmatics. European Respiratory Journal, 32(2), 362-371. https://doi.org/10.1183/09031936.00119307
Ward, J. E. ; Harris, T. ; Bamford, T. ; Mast, A. ; Pain, M. C.F. ; Robertson, C. ; Smallwood, D. ; Tran, T. ; Wilson, J. ; Stewart, A. G. / Proliferation is not increased in airway myofibroblasts isolated from asthmatics. In: European Respiratory Journal. 2008 ; Vol. 32, No. 2. pp. 362-371.
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Ward, JE, Harris, T, Bamford, T, Mast, A, Pain, MCF, Robertson, C, Smallwood, D, Tran, T, Wilson, J & Stewart, AG 2008, 'Proliferation is not increased in airway myofibroblasts isolated from asthmatics', European Respiratory Journal, vol. 32, no. 2, pp. 362-371. https://doi.org/10.1183/09031936.00119307

Proliferation is not increased in airway myofibroblasts isolated from asthmatics. / Ward, J. E.; Harris, T.; Bamford, T.; Mast, A.; Pain, M. C.F.; Robertson, C.; Smallwood, D.; Tran, T.; Wilson, J.; Stewart, A. G.

In: European Respiratory Journal, Vol. 32, No. 2, 08.2008, p. 362-371.

Research output: Contribution to journalArticleResearchpeer-review

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AU - Harris, T.

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