Am. J. Respir. Crit. Care Med., Vol 150, No. 1, 07 1994, 214-217.
Cell proliferation in the bronchial mucosa of asthmatics and chronic bronchitics
P Demoly, J Simony-Lafontaine, P Chanez, JL Pujol, N Lequeux, FB Michel and J Bousquet
Clinique des Maladies Respiratoires, Hopital Arnaud de Villeneuve, Centre Hospitalier Universitaire, Montpellier, France.
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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Copyright © 1994 American Thoracic Society
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