Role of Endotoxin in Tumor Necrosis Factor a Expression from Alveolar Macrophages Treated with Urban Air Particles

Abstract

The effects of urban air and diesel particles on inflammatory cytokine gene expression, tumor necrosis factor α (TNF-α) in particular, were studied in rat alveolar macrophages. TNF-α, interleukin (IL)-1, IL-6, cytokine-induced neutrophil chemoattractanl (CINC), and macrophage inflammatory protein (MIP)-2 gene expression and TNF-α secretion were increased in cells treated with 50 to 200 μg/mL of urban air particles in a concentration-related manner. There was no cytokine induction by diesel particles al any of the concentrations tested. Cytokine expression was not related to reactive oxygen species since antioxidants, such as catalase, TMTU, or DMSO, had no effect on TNF-a 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, hut 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.