Expression of ErbB receptors and mucins in the airways of long term current smokers
- R A O’Donnell1,
- A Richter1,
- J Ward1,
- G Angco1,
- A Mehta1,
- K Rousseau2,
- D M Swallow2,
- S T Holgate1,
- R Djukanovic1,
- D E Davies1,
- S J Wilson1
- 1Respiratory Cell and Molecular Biology, Division of Infection, Inflammation and Repair, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK
- 2Galton Laboratory, Biology Department, University College London, London NW1 2HE, UK
- Correspondence to:
Dr D E Davies
The Brooke Laboratories, Division of Infection, Inflammation and Repair, School of Medicine, Southampton General Hospital, Southampton, SO16 6YD, UK;
- Received 12 May 2004
- Accepted 23 August 2004
Background: Airway epithelial goblet cell hyperplasia is known to occur in chronic smokers. Although the epidermal growth factor receptor has been implicated in this process, neither ErbB receptor expression nor the mucosecretory phenotype of the epithelium have been characterised in current smokers.
Methods: Bronchial biopsies obtained from non-smokers (n = 10) and current smokers, with or without chronic obstructive pulmonary disease (n = 51), were examined immunohistochemically to measure the expression of epidermal growth factor receptor, ErbB2, ErbB3, ErbB4 and mucin subtypes (MUC2, MUC5AC and MUC5B) in the bronchial epithelium. The results were correlated with neutrophil counts measured in the airway wall and induced sputum.
Results: Epidermal growth factor receptor, ErbB3 and MUC5AC expression, in addition to PAS staining, were significantly increased in all smokers compared with non-smokers, irrespective of the presence of chronic obstructive pulmonary disease. MUC5AC expression was significantly associated with both PAS staining and ErbB3 expression; no correlation was observed between either mucin or ErbB receptor expression and neutrophil counts.
Conclusions: The results suggest that long term current smoking induces enhanced epidermal growth factor receptor, ErbB3, and MUC5AC expression in vivo; these increases are not associated with the presence of neutrophilic inflammation. ErbB receptors may contribute to epithelial responses to cigarette smoke.
This work was supported by AstraZeneca.