BrooklynDodger(s) comment: This raises a concern that complexity could be used in future to obfuscate regulation. Would be good to have some notion of relative potency, although some of these are granular and some have some solubility. It's a bit of a surprise that ZnCl2 is up there with LPS. Hard to think of what could be used as a negative control.
ToxicologyVolume 259, Issues 1-2, 2 May 2009, Pages 46-53
ToxicologyVolume 259, Issues 1-2, 2 May 2009, Pages 46-53
Cytokine and chemokine expression patterns in lung epithelial cells exposed to components characteristic of particulate air pollution
J. Øvrevik, a, , M. Låga, J.A. Holmea, P.E. Schwarzea and M. Refsnesa
aDepartment of Air Pollution and Noise, Division of Environmental Medicine, Norwegian
Abstract
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.
Keywords: Air pollution; Lung; Epithelium; Inflammation; Cytokines; Gene expression
J. Øvrevik, a, , M. Låga, J.A. Holmea, P.E. Schwarzea and M. Refsnesa
aDepartment of Air Pollution and Noise, Division of Environmental Medicine, Norwegian
Abstract
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.
Keywords: Air pollution; Lung; Epithelium; Inflammation; Cytokines; Gene expression
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