Airway fibrosis in rats induced by vanadium pentoxide

Laboratories of 1  Pulmonary Pathobiology, 2  Experimental Pathology, and 3  Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709 Vanadium pentoxide (V 2 O 5 ) is a cause of occupational asthma and bronchitis. We...

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Bibliographic Details
Published in:American journal of physiology. Lung cellular and molecular physiology 2000-01, Vol.278 (1), p.209-L216
Main Authors: Bonner, James C, Rice, Annette B, Moomaw, Cindy R, Morgan, Daniel L
Format: Article
Language:English
Subjects:
Animals
Bronchi - drug effects
Bronchi - pathology
Bronchi - physiopathology
Epithelium - pathology
Epithelium - physiopathology
Fibroblasts - pathology
Fibrosis
Male
Muscle, Smooth - pathology
Rats
Rats, Sprague-Dawley
Vanadium Compounds - pharmacology
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Summary:Laboratories of 1  Pulmonary Pathobiology, 2  Experimental Pathology, and 3  Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709 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. asthma; myofibroblasts; smooth muscle cell; collagen; metals
ISSN:1040-0605
1522-1504
DOI:10.1152/ajplung.2000.278.1.l209