Role of endotoxin in tumor necrosis factor alpha expression from alveolar macrophages treated with urban air particles

被引:58
作者
Dong, WM
Lewtas, J
Luster, MI
机构
[1] US EPA, HUMAN STUDIES DIV, CHAPEL HILL, NC USA
[2] NIOSH, TOXICOL & MOL BIOL BRANCH, MORGANTOWN, WV USA
关键词
alveolar macrophage; diesel particles; endotoxin; inflammatory cytokines; lung inflammation; urban air particles;
D O I
10.3109/01902149609046043
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
The effects of urban air and diesel particles on inflammatory cytokine gene expression, tumor necrosis factor alpha (TNF-alpha) in particular, were studied in rat alveolar macrophages. TNF-alpha, interleukin (IL)-1, IL-6, cytokine-induced neutrophil chemoattractant (CINC), and macrophage inflammatory protein (MIP)-2 gene expression and TNF-alpha secretion were increased in cells treated with 50 to 200 mu g/mL of urban air particles in a concentration-related manner. There was no cytokine induction by diesel particles at any of the concentrations tested. Cytokine expression was not related to reactive oxygen species since antioxidants, such as catalase, TMTU, or DMSO, had not effect on TNF-alpha secretion. However, cytokine induction by urban air particles was completely prevented by polymyxin B, an antibiotic capable of neutralizing bacterial lipopolysaccharide (LPS) activities. Furthermore, LPS was detected on the urban air particles, but not on diesel particle. These results suggest that activation of cytokine gene expression and secretion in rat alveolar macrophages by urban air particles is due to the presence of endotoxin on the particles.
引用
收藏
页码:577 / 592
页数:16
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