Present address: GlaxoSmithKline, Translational Medicine and Technology, Clinical Pharmacology and Discovery Medicine, Room 5123, 891-995 Greenford Road, Greenford, Middlesex UB6 0HE.
FITC-induced murine pulmonary inflammation: CC10 up-regulation and concurrent Shh expression
Version of Record online: 2 JAN 2013
© The Author(s) Journal compilation © 2005 International Federation for Cell Biology
Cell Biology International
Volume 29, Issue 10, pages 868–876, October 2005
How to Cite
Fisher, C. E., Ahmad, S. A., Fitch, P. M., Lamb, J. R. and Howie, S. E.M. (2005), FITC-induced murine pulmonary inflammation: CC10 up-regulation and concurrent Shh expression. Cell Biology International, 29: 868–876. doi: 10.1016/j.cellbi.2005.07.002
- Issue online: 2 JAN 2013
- Version of Record online: 2 JAN 2013
- Received 14 December 2004; revised 13 June 2005; accepted 13 July 2005
- Clara cells;
- Pulmonary inflammation
We describe an immunohistochemical study of the acute and chronic effects of fluorescein isothiocyanate (FITC) on Sonic hedgehog (Shh) expression and Clara cell secretory protein (CC10) up-regulation in murine lung. FITC was dissolved in PBS and instilled non-surgically into adult mouse lungs via the trachea. During the acute phase (120 h) of the FITC response, CC10 staining within Clara cells increased markedly but the protein did not leak into the tissue spaces or the airways, and no fibrosis was apparent. An immune response was evident, characterised by infiltrating T and B lymphocytes. There was no concomitant expression of Shh. During the chronic phase (6 months post-instillation), significant tissue degeneration was observed in the airways. There was moderate to severe fibrosis in the lung fields that stained positively for FITC and significant inflammatory cell infiltrate was observed. Shh was expressed, and CC10 showed multiple sites of diffuse staining consistent with release from Clara cells into alveolar air spaces. PBS controls showed no fibrosis after 6 months, but there was positive Shh staining below the airway epithelia and minimal extracellular CC10 staining. The results may throw some light on the role of CC10 in pulmonary inflammation. The relationship of Shh expression and CC10 leakage to lung damage and repair is discussed.