Cytokine and chemokine expression patterns in lung epithelial cells exposed to components characteristic of particulate air pollution

Airborne particulate matter (PM) has a complex composition, and the relative contribution of different compounds to PM-induced effects is only partly understood. The present study compared the capability of selected components commonly found in PM, to induce pro-inflammatory responses in lung epithelial cells. Ultrafine carbon black (ufCB), ZnCl2, FeSO4, 1-nitropyrene (1-NP), lipopolysaccharide (LPS), and crystalline silica (positive control) were screened for effects on the expression of 84 inflammation-related genes in the bronchial epithelial cell line, BEAS-2B. A total of 22 genes were up-regulated by one or more of the tested compounds, and 5 cytokine and 11 chemokine genes were selected for further studies. After 10 h exposure, silica induced significantly increased expression of CCL20, CXCL1/-3/-8/-10/-11, lymphotoxin (LT)β and interleukin (IL)-6; ufCB induced CXCL8/-10 and -11; ZnCl2 induced CCL11/-20/-26, CXCL1/-5/-8/-14 and tumor necrosis factor (TNF)-α; FeSO4 induced a weak up-regulation of CXCL8 and TNF-α; LPS induced CCL20, CXCL1/-5/-8/-10/-11, LTβ and IL-6; and 1-NP induced expression of CCL20, CXCL1/-3/-8, TNF-α and IL-6. Despite obvious differences, all compounds induced response-patterns that correlated relatively well with that of silica, the positive control. The predominant response appeared to be increased gene expression of neutrophil-recruiting CXC-chemokines. CXCL8 was the only gene induced by all tested PM-components, the most up-regulated on average, and also dominating the gene-expression patterns induced by coarse PM. The data show quantitative, and to a certain extent qualitative differences in cytokine/chemokine gene-expression profiles of the compounds tested. However, there were also striking similarities in the response-patterns induced by these physically/chemically widely different compounds.