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Updated: Aug 8, 2026

Primary Human Bronchial Epithelial Cells Grown from Explants
Published on: March 27, 2010
Cell proliferation in the bronchial mucosa of asthmatics and chronic bronchitics
P Demoly1, J Simony-Lafontaine, P Chanez
1Clinique des Maladies Respiratoires, Hopital Arnaud de Villeneuve, Centre Hospitalier Universitaire, Montpellier, France.
Insights
Bronchial cell proliferation is low in non-smokers, including asthmatics. Tobacco smoking significantly increases cell proliferation, potentially causing metaplasia in chronic bronchitis.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Respiratory Pathology
Background:
- Cellular proliferation in the bronchial epithelium is a key factor in chronic inflammatory diseases.
- While normal bronchial epithelium has low cell cycling, asthma and chronic bronchitis may involve increased proliferation.
- Proliferating Cell Nuclear Antigen (PCNA) is a biomarker for identifying cycling cells.
Purpose of the Study:
- To quantify Proliferating Cell Nuclear Antigen (PCNA)-positive cells in bronchial biopsies across different subject groups.
- To investigate the relationship between smoking, asthma, chronic bronchitis, and bronchial epithelial cell proliferation.
- To determine if bronchial mucosa exhibits hyperproliferation in non-smokers, even with asthma.
Main Methods:
- Immunohistochemistry was used to detect PCNA-positive cells in bronchial biopsies.
- Labeling Index (LI) was calculated for basal cells in healthy non-smokers, healthy smokers, non-smoking asthmatics, smoking asthmatics, and chronic bronchitis patients.
- Statistical analysis, including correlation tests, was performed to assess relationships between PCNA positivity and clinical factors.
Main Results:
- PCNA-positive basal cells were found in 1/11 healthy non-smokers, 0/7 healthy smokers, 2/30 non-smoking asthmatics, 2/6 smoking asthmatics, and 11/18 chronic bronchitis patients.
- PCNA positivity in smokers correlated with tobacco consumption (Rho = 0.62).
- In chronic bronchitis patients, PCNA positivity correlated with the degree of metaplasia (tau = 0.815).
Conclusions:
- Bronchial mucosa in non-smokers, including asthmatics, does not appear to be hyperproliferative.
- Tobacco smoking significantly increases bronchial epithelial cell proliferation (PCNA immunoreactivity).
- Increased proliferation due to smoking may contribute to the metaplasia observed in chronic bronchitis.
Abstract:
In chronic inflammatory diseases, cells are recruited but may also derive from local proliferation. In normal bronchial epithelium, under 5% of cells are in cycle but in asthma and chronic bronchitis, proliferation may occur. Cycling cells can be identified by immunohistochemistry using PC10 monoclonal antibody (Proliferating Cell Nuclear Antigen, PCNA). We enumerated PCNA-positive cells (labeling index = LI) in bronchial biopsies of 11 healthy non-smokers (HNS), seven healthy smokers (HS), 30 non-smoking asthmatics (NSA), six smoking asthmatics (SA) and 18 chronic bronchitics (CB). Twenty non-small cell lung cancer patients were used as positive control subjects. Ciliated and secretory cells were PCNA-negative. Basal cells were PCNA-positive in one of the 11 HNS (LI = 0.18 +/- 0.60), none of the seven HS, two of the 30 NSA (LI = 0.05 +/- 0.20), two of the six SA (LI = 2.4 +/- 4.3) and 11 of the 18 CB (LI = 12 +/- 20). In smokers, PCNA positivity correlated with tobacco consumption (Rho = 0.62, p < 0.0008) and in patients with chronic bronchitis, with the degree of metaplasia (tau = 0.815, p < 0.0001). The submucosa of most subjects showed no PCNA immunoreactivity. These findings suggest that the bronchial mucosa of nonsmokers is not hyperproliferative, even in asthmatics. Tobacco smoking increases PCNA immunoreactivity, possibly leading to the metaplasia of chronic bronchitis.
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