Journal of Environmental Pathology, Toxicology and Oncology

ISSN for PRINT: 0731-8898

For Online Access

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2002, Volume21

Issue 4

80 pages

Issue price - $160.00

Liying Wang
National Institute for Occupational Safety and Health, Pathology and Physiology Research Branch, Morgantown, WV 26505

Djordje Medan
West Virginia University Health Sciences Center, Department of Basic Pharmaceutical Sciences, Morgantown, WV 26506

Robert Mercer
National Institute for Occupational Safety and Health, Pathology and Physiology Research Branch, Morgantown, WV 26505

Xianglin Shi
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown,WV

Chuanshu Huang
Nelson Institute of Environment Medicine, New York University School of Medicine, New York, NY 10061

Vincent Castranova
National Institute for Occupational Safety and Health: Health Effects Laboratory Division, Morgantown,WV

Min Ding
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown,WV

Yongyut Rojanasakul
West Virginia University Health Sciences Center, Department of Basic Pharmaceutical Sciences, Morgantown, WV 26506

Pulmonary exposure to airborne vanadium and vanadium-containing compounds is associated with acute pulmonary inflammation, characterized by a rapid influx of neutrophilic polymorphonuclear leukocytes with a peak response at 6 hours and resolution by 3 days. We hypothesized that neutrophil apoptosis is involved in the resolution of vanadium-induced lung inflammation. To test this hypothesis, mice were exposed to inspired vanadium or saline control and the bronchoalveolar lavage (BAL) cells were examined at various times for apoptosis using terminal deoxyribonucleotidyl transferase-mediated nick end labeling (TUNEL). Control mice showed only resident alveolar macrophages in the BAL with no evidence of apoptosis. In contrast, vanadium-treated mice showed clear apoptosis of BAL cells, which were predominantly neutrophils. The number of apoptotic cells gradually increased and reached a maximal level by 24 hours with subsequent decline. After 24 hours, when the vanadium-induced lung inflammation was in the resolution phase, we observed an increased number of alveolar macrophages in BAL and the engulfment of apoptotic bodies by these macrophages. At 72 hours, the total number of neutrophils in BAL fell to the baseline level, and the number of apoptotic cells was reduced. Clearance of the apoptotic product was demonstrated by the presence of apoptotic bodies in the cytoplasm of alveolar macrophages. We conclude that apoptosis of neutrophils and clearance by alveolar macrophages are important mechanisms in the resolution of vanadium-induced lung inflammation.

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