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), ZnCl(2), FeSO(4), 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 10h exposure, silica induced significantly increased expression of CCL20, CXCL1/-3/-8/-10/-11, lymphotoxin (LT)beta and interleukin (IL)-6; ufCB induced CXCL8/-10 and -11; ZnCl(2) induced CCL11/-20/-26, CXCL1/-5/-8/-14 and tumor necrosis factor (TNF)-alpha; FeSO(4) induced a weak up-regulation of CXCL8 and TNF-alpha; LPS induced CCL20, CXCL1/-5/-8/-10/-11, LTbeta and IL-6; and 1-NP induced expression of CCL20, CXCL1/-3/-8, TNF-alpha 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.
Ovrevik
J
J
Department of Air Pollution and Noise, Division of Environmental Medicine, Norwegian Institute of Public Health, Norway. johan.ovrevik@fhi.no
Låg
M
M
Holme
J A
JA
Schwarze
P E
PE
Refsnes
M
M
D000393:Air Pollutants / Q000737:chemistry / Q000633:toxicity*; D001980:Bronchi / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D002461:Cell Line, Transformed; D045744:Cell Line, Tumor; D018925:Chemokines / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D008168:Lung / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008175:Lung Neoplasms / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism; D012822:Silicon Dioxide / Q000633:toxicity; D015854:Up-Regulation / Q000187:drug effects*
D000393:Air Pollutants; D018925:Chemokines; D016207:Cytokines; D012822:Silicon Dioxide