Airway fibrosis in rats induced by vanadium pentoxide

Vanadium pentoxide (V2O5) is a cause of occupational asthma and bronchitis. We previously reported that intratracheal instillation of rats with V2O5 c auses 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. Physi ol. 274: L72-L80, 1998). In this report, we show that intratracheal instill ation of V2O5 induces airway remodeling similar to that observed in individ uals with asthma. These changes include airway smooth muscle cell thickenin g, mucous cell metaplasia, and airway fibrosis. The transient appearance of peribronchiolar myofibroblasts, which were desmin and vimentin positive, c oincided with a twofold increase in the thickness of the airway smooth musc le layer at day 6 after instillation and preceded the development of airway fibrosis by day 15. The number of nuclear profiles within the smooth muscl e layer also increased twofold after V2O5 instillation, suggesting that hyp erplasia accounted for thickening of the smooth muscle layer. The majority of cells incorporating bromodeoxyuridine at day 3 were located in the conne ctive tissue surrounding the airway smooth muscle wall that was positive fo r vimentin and desmin. These data suggest that myofibroblasts are the princ ipal proliferating cell type that contributes to the progression of airway fibrosis after V2O5 injury.