期刊
TOXICOLOGY
卷 284, 期 1-3, 页码 34-41出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.tox.2011.03.012
关键词
T-2 toxin; p38 MAPK; Aryl hydrocarbon receptor; CYP1A1; IL-8; Caco-2
资金
- Helmholtz Alliance on Systems Biology
- Deutsche Bundesstiftung Umwelt [20004/740]
T-2 toxin (T-2) is a secondary metabolite produced by various mould species of the genus Fusarium and a common contaminant detectable in staple foods of cereal origin. In the present study the impact of this mycotoxin on the inflammatory response of the intestinal epithelial cell line Caco-2 was examined by measuring interleukin (IL)-8 secretion. A T-2 concentration dependent IL-8 up-regulation was detected in IL-1 beta stimulated and unstimulated Caco-2 cells. To elucidate the possible underlying molecular mechanism of this conditional T-2-provoked IL-8 induction, a possible involvement of the aryl hydrocarbon receptor (AHR) and the mitogen-activated protein kinase (MAPK) pathway was investigated. Like benzo[a]-pyrene (B[a]P), a well known AHR ligand, T-2 led to cytochrome P450 1A1 (CYP1A1)mRNA expression in Caco-2 cells, which could be inhibited by the AHR antagonist resveratrol. However, resveratrol did not influence T-2-dependent IL-8 induction. Since T-2 did not lead to AHR-translocation in stably GFP-AHR-transfected cells, an AHR dependency of T-2-triggered IL-8 induction could be excluded. But finally, up to a total inhibition of T-2-induced IL-8 was obtained using p38 inhibitors. Therefore, we conclude that p38 MAPK is responsible for mediating the inflammatory properties of the type A trichothecene T-2. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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