Particulate matter induces cytokine expression in human bronchial epithelial cells

The present study was designed to determine cytokines produced by primary h uman bronchial epithelial cells (HBECs) exposed to ambient air pollution pa rticles (EHC-93). Cytokine messenger RNA (mRNA) was measured using a ribonu clease protection assay and cytokine protein production by enzyme-linked im munosorbent 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), granulo cyte macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-1 alph a, and IL-8 were increased after exposure to PM10, and this increase was do se-dependent between 100 (P < 0.05) and 500 (P < 0.05) mug/ml of PM10 expos ure. The concentrations of LIP, GM-CSF, IL-1 beta, and IL-8 protein measure d 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 cytoki ne mRNA levels compared with control values and were significantly lower co mpared 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 p rimary HBECs exposed to ambient PM10 produce proinflammatory mediators that contribute to the local and systemic inflammatory response, and we specula te that these mediators may have a role in the pathogenesis of cardiopulmon ary disease associated with particulate air pollution.