Journal article

Publication year: 2008

Pages: 813-820

Journal: Inhalation Toxicology

Volume number: 20

Issue number: 9

ISSN: 0895-8378

DOI Link: https://doi.org/10.1080/08958370802020810

Publisher: Taylor and Francis Group

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- 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-B 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- B and p38 MAP kinase and a release of the chemokine MCP-1. In the presence of IKK-NBD, a specific NF- 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- B and MAPK pathways.

Harvard Citation style: Röder-Stolinski, C., Fischäder, G., Oostingh, G., Eder, K., Duschl, A. and Lehmann, I. (2008) Chlorobenzene Induces the NF-κB and p38 MAP Kinase Pathways in Lung Epithelial Cells, Inhalation Toxicology, 20(9), pp. 813-820. https://doi.org/10.1080/08958370802020810

APA Citation style: Röder-Stolinski, C., Fischäder, G., Oostingh, G., Eder, K., Duschl, A., & Lehmann, I. (2008). Chlorobenzene Induces the NF-κB and p38 MAP Kinase Pathways in Lung Epithelial Cells. Inhalation Toxicology. 20(9), 813-820. https://doi.org/10.1080/08958370802020810