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156455 
Journal Article 
Particulate matter induces cytokine expression in human bronchial epithelial cells 
Fujii, T; Hayashi, S; Hogg, JC; Vincent, R; Van Eeden, SF 
2001 
Yes 
American Journal of Respiratory Cell and Molecular Biology
ISSN: 1044-1549
EISSN: 1535-4989 
25 
3 
265-271 
English 
11588002 
WOS:000171665000001 
The present study was designed to determine cytokines produced by primary human bronchial epithelial cells (HBECs) exposed to ambient air pollution particles (EHC-93). Cytokine messenger RNA (mRNA) was measured using a ribonuclease protection assay and cytokine protein production by enzyme-linked immunosorbent assay. Primary HBECs were freshly isolated from operated lung, cultured to confluence, and exposed to 10 to 500 mug/ml of a suspension of ambient particulate matter with a diameter of less than 10 mum (PM10) for 2, 8, and 24 h. The mRNA levels of leukemia inhibitory factor (LIF), granulocyte macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-1 alpha, and IL-8 were increased after exposure to PM10, and this increase was dose-dependent between 100 (P < 0.05) and 500 (P < 0.05) mug/ml of PM10 exposure. The concentrations of LIP, GM-CSF, IL-1 beta, and IL-8 protein measured in the supernatant collected at 24 h increased in a dose-dependent manner and were significantly higher than those in the control nonexposed cells. The soluble fraction of the PM10 (100 mug/ml) did not increase these cytokine mRNA levels compared with control values and were significantly lower compared with HBECs exposed to 100 mug/ml of PM10 (LIF, IL-8, and IL-1 beta; P < 0.05), except for GM-CSF mRNA (P = not significant). We conclude that primary HBECs exposed to ambient PM10 produce proinflammatory mediators that contribute to the local and systemic inflammatory response, and we speculate that these mediators may have a role in the pathogenesis of cardiopulmonary disease associated with particulate air pollution.