Effects of deoxynivalenol (vomitoxin) on the humoral and cellular immunity of mice

Tryphonas, Helen; Iverson, F.; So, Ying Peng; Nera, E.A.; McGuire, Peter; OʼGrady, Lois F.; Clayson, David B.; Scott, Peter

doi:10.1016/0378-4274(86)90096-2

Cited by 76 publications

(33 citation statements)

References 10 publications

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“…These reports suggest that the data of immune dysfunction as well as cytotoxicity are important in risk analysis for trichothecene mycotoxins and immune cells are the primary target for this mycotoxins (Bondy and Pestka 2000). Therefore, susceptibility to infections caused by other food-borne pathogens, such as Listeria monocytogenes, is enhanced by DON (Tryphonas et al 1986).…”

Section: Introductionmentioning

confidence: 99%

Effect of a combination of deoxynivalenol and nivalenol on lipopolisaccharide-induced nitric oxide production by mouse macrophages

et al. 2010

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Deoxynivalenol (DON) and nivalenol (NIV) are trichothecene mycotoxins produced by Fusarium fungi as secondary metabolites. Both compounds have the immunotoxic effects that the productions of inflammatory mediators by activated macrophages is disturbed. Co-contamination with DON and NIV can occur; however, the effects of simultaneous contamination are not well known. The present study investigated the combined effects of DON and NIV on nitric oxide (NO) production by mouse macrophages stimulated with lipopolisaccharide (LPS). The inhibitory effect of DON and NIV on NO release from activated macrophages has already been reported as an appropriate indicator of immunotoxic effect of the both compounds. LPS-induced NO production in macrophages was inhibited by both of these toxins individually in a dose-dependent manner, and toxin mixtures at the same concentration inhibited NO production in the same manner. In addition, there were no unique inhibitory effects on LPS-induced NO production in macrophages in the presence of mixtures of various molar ratios. These results suggest that the combined effects of DON and NIV can be predicted based on addition of each compound alone.

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Section: Introductionmentioning

confidence: 99%

Effect of a combination of deoxynivalenol and nivalenol on lipopolisaccharide-induced nitric oxide production by mouse macrophages

et al. 2010

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“…Reproductive defects in mice caused by trichothecenes include embryo or foetal toxicity caused by T-2 toxin (Rousseaux et al 1986), increased postnatal mortality caused by DON (Khera et al 1984) and intrauterine growth retardation caused by NIV (Ito et al 1988). DON increased the susceptibility of mice to infections (Tryphonas et al 1986). DAS exposure caused suppression in chicken macrophage phagocitic function (Qureshi et al 1998).…”

Section: Gross Toxic Effects Of Trichothecenes On Animalsmentioning

confidence: 99%

Effects of trichothecene mycotoxins on eukaryotic cells: A review

Rocha

Ansari²,

Doohan³

2005

Food Additives and Contaminants

492

298

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The major products of the trichothecene mycotoxin biosynthetic pathway produced in a species-and sometimes isolatespecific manner by cereal-pathogenic Fusarium fungi include T-2 toxin, diacetoxyscirpenol, deoxynivalenol and nivalenol. This paper briefly reviews the major effects of such trichothecenes on the gross morphology, cytology and molecular signalling within eukaryotic cells. The gross toxic effects of select trichothecenes on animals include growth retardation, reduced ovarian function and reproductive disorders, immuno-compromization, feed refusal and vomiting. The phytotoxic effects of deoxynivalenol on plants can be summarized as growth retardation, inhibition of seedling and green plant regeneration. Trichothecenes are now recognized as having multiple inhibitory effects on eukaryote cells, including inhibition of protein, DNA and RNA synthesis, inhibition of mitochondrial function, effects on cell division and membrane effects. In animal cells, they induce apoptosis, a programmed cell death response. Current knowledge about the eukaryotic signal transduction cascades and downstream gene products activated by trichothecenes is limited, especially in plants. In mammalian cells, certain trichothecenes trigger a ribotoxic stress response and activate mitogen-activated protein kinases. DON mediates the inflammatory response by modulating the binding activities of specific transcription factors and subsequently inducing cytokine gene expression. Several genes are up-regulated in wheat in response to trichothecene mycotoxins; the significance, if any, of these genes in the host response to trichothecenes has yet to be elucidated.

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“…In addition, previous studies have demonstrated that DON has adverse effects in immune cells including B and T cells, natural killer cells and macrophages (Instanes and Hetland, 2004;Pestka, 2008), and causes immune dysfunction (Pestka and Smolinski, 2005). Trichothecene mycotoxins can either enhance or suppress resistance to pathogens such as Salmonella (Tai and Pestka, 1990;Ziprin and Elissalde, 1990), reovirus (Li et al, 2007) and Listeria (Tryphonas et al, 1986). In particular, it has been revealed that DON induces innate immune cell cytotoxicity and dysregulates the innate immune responses (Instanes and Hetland, 2004;Pestka and Smolinski, 2005;Pestka, 2008;Sugiyama et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

NF-κB activation via MyD88-dependent Toll-like receptor signaling is inhibited by trichothecene mycotoxin deoxynivalenol

et al. 2016

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-Macrophages induce the innate immunity by recognizing pathogens through Toll-like receptors (TLRs), which sense pathogen-associated molecular patterns. Myeloid differentiation factor 88 (MyD88), which is an essential adaptor molecule for most TLRs, mediates the induction of inflammatory cytokines through nuclear factor κB (NF-κB). Trichothecene mycotoxin deoxynivalenol (DON) shows immunotoxic effects by interrupting inflammatory mediators produced by activated macrophages. The present study investigates the effect of DON on NF-κB in activated macrophages through MyD88-dependent pathways. DON inhibited NF-κB-dependent reporter activity induced by MyD88-dependent TLR agonists. In addition, lipopolysaccharide-induced phosphorylation of interleukin-1 receptor-associated kinase 1 and inhibitor κBα were attenuated by DON. Furthermore, DON downregulated the expression level of MyD88. These results suggest that DON inhibits NF-κB activation in macrophages stimulated with TLR ligands via MyD88-dependent TLR signals. Therefore exposure to DON may lead to the inhibition of MyD88-dependent pathway of TLR signaling.

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Effects of deoxynivalenol (vomitoxin) on the humoral and cellular immunity of mice

Cited by 76 publications

References 10 publications

Effect of a combination of deoxynivalenol and nivalenol on lipopolisaccharide-induced nitric oxide production by mouse macrophages

Effect of a combination of deoxynivalenol and nivalenol on lipopolisaccharide-induced nitric oxide production by mouse macrophages

Effects of trichothecene mycotoxins on eukaryotic cells: A review

NF-κB activation via MyD88-dependent Toll-like receptor signaling is inhibited by trichothecene mycotoxin deoxynivalenol

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