Paper Title
T2 Toxin Abrogates LPS-Induced Proinflammatory Response in Hepg2 Liver Cells: Evidence for A Novel Mechanism Involving Mitochondrial Stress Responses

Abstract
The type A tricothecene T2 toxin is a principal mycotoxin known to inhibit protein synthesis. Its toxicity is mediated by mitochondrial dysfunction and oxidative stress. Mitochondrial stress and generation of reactive oxygen species are involved in the signalling events controlling the activation of the inflammatory transcription factor NF-κB. The aim was to assess if these pathways are involved in T2 toxin-mediated effects on LPS-induced inflammatory responses. HepG2 cells were stimulated with Escherichia coli LPS in the presence and absence of T2 toxin. T2 toxin inhibited the activation of NF-κB and up-regulated mitochondrial stress responses. In conclusion, T2 toxin potently inhibits expression of LPS-induced inflammatory responses via mechanisms that involve modulation and activity of mitochondrial stress proteins. Index Terms— LPS, Mitochondria, NFκB, T2 toxin