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Journal of Environmental Pathology, Toxicology and Oncology

Published 4 issues per year

ISSN Print: 0731-8898

ISSN Online: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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

Volume 21, Issue 4, 2002, 8 pages
DOI: 10.1615/JEnvironPatholToxicolOncol.v21.i4.30
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ABSTRACT

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.

CITED BY
  1. Yun Jeong H, Henson Peter M, Tuder Rubin M, Phagocytic clearance of apoptotic cells: role in lung disease, Expert Review of Respiratory Medicine, 2, 6, 2008. Crossref

  2. Leonard Stephen S., Harris Gabriel K., Shi Xianglin, Metal-induced oxidative stress and signal transduction, Free Radical Biology and Medicine, 37, 12, 2004. Crossref

  3. Cohen Mitchell D., Sisco Maureen, Prophete Colette, Yoshida Kotaro, Chen Lung-chi, Zelikoff Judith T., Smee Jason, Holder Alvin A., Stonehuerner Jacqueline, Crans Debbie C., Ghio Andrew J., Effects of metal compounds with distinct physicochemical properties on iron homeostasis and antibacterial activity in the lungs: chromium and vanadium, Inhalation Toxicology, 22, 2, 2010. Crossref

  4. Wang Liying, Bowman Linda, Lu Yongju, Rojanasakul Yon, Mercer Robert R., Castranova Vince, Ding Min, Essential role of p53 in silica-induced apoptosis, American Journal of Physiology-Lung Cellular and Molecular Physiology, 288, 3, 2005. Crossref

  5. Liang Jiurong, Jung Yoosun, Tighe Robert M., Xie Ting, Liu Ningshan, Leonard Maura, Gunn Michael Dee, Jiang Dianhua, Noble Paul W., A macrophage subpopulation recruited by CC chemokine ligand-2 clears apoptotic cells in noninfectious lung injury, American Journal of Physiology-Lung Cellular and Molecular Physiology, 302, 9, 2012. Crossref

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