Abstract
Fumonisin B 1 (FB 1), a mycotoxin produced primarily by Fusarium veticillioides and related fungi, is a carcinogen and causative agent of various animal diseases. Our previous studies indicated the involvement of tumor necrosis factor-α (TNFα) in FB 1-induced hepatotoxicity. Male B6,129 mice (five/group) were injected subcutaneously with vehicle or 2.25 mg/kg/day of FB 1 for 5 days and sampled 1 day after the last treatment. FB 1 treatment caused an increased expression of TNFα, interferon γ (IFNγ) and interleukin (IL)-12 p40 in liver without any changes in kidney or spleen, suggesting the localized site of their production. IL-1β cytokine expression was increased in liver and kidney after FB 1 exposure. Cells involved in TNFα production after FB 1 treatment in liver were identified as Kupffer cells. FB 1 increased alanine aminotransferase in plasma and increased apoptotic cells in liver. Selective increase in proinflammatory T helper (Th)1-cytokines (IL-12 and IFNγ) and TNFα with no alteration in Th2-cytokines (IL-4, IL-6 and IL-10) suggest the involvement of IL-12, produced by Kupffer cells, in induction of IFNγ production by natural killer (NK) cells and/or NK1 + T cells, which can undergo a positive amplification loop with TNFα produced by macrophages or other hepatic cells to elicit the toxic reaction.
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