interleukin-8 and nivalenol

Topics: Cell Line; Cell Survival; Epithelial Cells; Humans; Interleukin-6; Interleukin-8; Respiratory System; Trichothecenes

Tricothecene mycotoxins, such as nivalenol, are toxic to leukocytes. To elucidate the molecular mechanism of nivalenol toxicity, we investigated the involvement of nuclear factor-κB (NF-κB) in nivalenol-induced cytotoxicity in HL60 cells using the NF-κB inhibitors pyrrolidinedithiocarbamate (PDTC) and dexamethasone. Cells were treated with the chemicals for 24h before assays were performed. Nivalenol elicited interleukin (IL)-8 secretion. IL-8 secretion was lower in cells concomitantly treated with nivalenol and NF-κB inhibitors than with nivalenol alone. Nivalenol reduced monocyte chemotactic protein (MCP)-1 secretion. MCP-1 secretion was higher in cells concomitantly treated with nivalenol and NF-κB inhibitors than with nivalenol alone. NF-κB inhibitors thus alleviated the effects of nivalenol, indicating that NF-κB is important for nivalenol-caused changes in cytokine secretion. Nivalenol hindered cell proliferation, and dexamethasone reduced this effect, suggesting that NF-κB contributes to cell proliferation. Thus, it appears that NF-κB is involved in nivalenol-induced toxicity in HL60 cells.

Topics: Anti-Inflammatory Agents; Antioxidants; Cell Proliferation; Cell Survival; Chemokine CCL2; Cytokines; Dexamethasone; HL-60 Cells; Humans; Interleukin-8; Mycotoxins; NF-kappa B; Proline; Thiocarbamates; Trichothecenes