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Journal of Environmental Pathology, Toxicology and Oncology
Impact-faktor: 1.625 5-jähriger Impact-Faktor: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN Druckformat: 0731-8898
ISSN Online: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v21.i4.30
8 pages

Role of Neutrophil Apoptosis in Vanadium-Induced Pulmonary Inflammation in Mice

Liying Wang
Pathology and Physiology Research Branch, National Institute for Occupational Safety and Health, Morgantown, West Virginia
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
Division of Nutritional Sciences, Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, KY; Center for Research on Environmental Disease, College of Medicine, University of Kentucky, Lexington, KY; Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, KY
Chuanshu Huang
New York University,Nelson Institute of Environment Medicine, New York University School of Medicine, New York, NY 10061
Vincent Castranova
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505
Min Ding
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505
Yongyut Rojanasakul
West Virginia University Health Sciences Center, Department of Basic Pharmaceutical Sciences, Morgantown, WV 26506

ABSTRAKT

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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