Details zur Publikation

Referenztyp Zeitschriften
DOI / URL Link
Titel (primär) Chlorobenzene induces the NF-kB and p38 MAP kinase pathways in lung epithelial cells
Autor Röder-Stolinski, C.; Fischäder, G.; Oostingh, G.J.; Eder, K.; Duschl, A.; Lehmann, I.;
Journal / Serie Inhalation Toxicology
Erscheinungsjahr 2008
Department IMMU;
Band/Volume 20
Heft 9
Sprache englisch;
Abstract Chlorobenzene is a volatile organic compound that is used as a solvent in many industrial settings and has been shown to be related with irritations of the respiratory tract. Exposure to chlorobenzene induces the release of monocyte chemoattractant protein 1 (MCP-1) by lung epithelial cells, a chemokine involved in inflammatory reactions. To characterize the underlying mechanisms we investigated the influence of chlorobenzene on the activation of two intracellular signalling pathways: the nuclear factor-kappa B (NF-k B) and the p38 mitogen-activated protein kinase (MAPK) pathways. Human lung epithelial cells (A549) were stimulated with tumor necrosis factor (TNF)- in the presence or absence of specific inhibitors of NF-kB or the p38 MAP kinase and exposed to chlorobenzene using an air-liquid cell culture system. Exposure of lung epithelial cells to chlorobenzene resulted in an activation of NF-k B and p38 MAP kinase and a release of the chemokine MCP-1. In the presence of IKK-NBD, a specific NF-k B inhibitor, or the inhibitors of the p38 MAP kinase SB 203580 and SB 202190, the chlorobenzene-related MCP-1 release was suppressed, suggesting an involvement of both pathways in the chlorobenzene induced expression of MCP-1. Our data show that the release of MCP-1 following chlorobenzene exposure is dependent on the NF-k B and MAPK pathways.
ID 1376
dauerhafte UFZ-Verlinkung
Röder-Stolinski, C., Fischäder, G., Oostingh, G.J., Eder, K., Duschl, A., Lehmann, I. (2008):
Chlorobenzene induces the NF-kB and p38 MAP kinase pathways in lung epithelial cells
Inhal. Toxicol. 20 (9), 813 - 820