Vanadium pentoxide (V(2)O(5)) is a cause of
occupational asthma and
bronchitis. We previously reported that intratracheal instillation of rats with V(2)O(5) causes
fibrosis of the lung parenchyma (J. C. Bonner, P. M. Lindroos, A. B. Rice, C. R. Moomaw, and D. L. Morgan. Am. J. Physiol. Lung Cell. Mol. Physiol. 274: L72-L80, 1998). In this report, we show that intratracheal instillation of V(2)O(5) induces
airway remodeling similar to that observed in individuals with
asthma. These changes include airway smooth muscle cell thickening, mucous cell
metaplasia, and airway
fibrosis. The transient appearance of peribronchiolar myofibroblasts, which were
desmin and
vimentin positive, coincided with a twofold increase in the thickness of the airway smooth muscle layer at day 6 after instillation and preceded the development of airway
fibrosis by day 15. The number of nuclear profiles within the smooth muscle layer also increased twofold after V(2)O(5) instillation, suggesting that
hyperplasia accounted for thickening of the smooth muscle layer. The majority of cells incorporating
bromodeoxyuridine at day 3 were located in the connective tissue surrounding the airway smooth muscle wall that was positive for
vimentin and
desmin. These data suggest that myofibroblasts are the principal proliferating cell type that contributes to the progression of airway
fibrosis after V(2)O(5) injury.