Deoxynivalenol and satratoxin G potentiate proinflammatory cytokine and macrophage inhibitory protein 2 induction by Listeria and Salmonella in the macrophage.

Deoxynivalenol and satratoxin G potentiate proinflammatory cytokine and macrophage inhibitory protein 2 induction by Listeria and Salmonella in the macrophage.
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DOI:
10.4315/0362-028x-69.6.1334
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发表时间:
2006-06
影响因子:
2
通讯作者:
E. Mbandi;J. Pestka
E. Mbandi;J. Pestka
中科院分区:
农林科学3区
文献类型:
--
作者:
E. Mbandi;J. Pestka

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食品和环境中遇到的微生物病原体和毒素造成的健康风险继续受到全世界的关注。这项研究的目的是验证毛霉菌毒素放大对食源性细菌病原体的炎症反应的假设。我们评价了脱氧雪腐镰刀菌烯醇(DON)和沙曲霉毒素G(SG)对单核细胞增生性李斯特氏菌和鼠伤寒沙门氏菌诱导的RAW 264.7小鼠巨噬细胞产生趋化因子和促炎细胞因子的能力。经灭活照射后的病原体悬液与巨噬细胞培养24 h后,诱导巨噬细胞抑制蛋白2(MIP-2)、白介素1β(IL-β)、白介素6(IL-6)和肿瘤坏死因子α(TNF-α)的最低李斯特氏菌浓度分别为0.01、0.01、1.0和1.0微克/毫升(P<0.05),最低沙门氏菌浓度分别为0.01、0.01、0.1和0.1微克/毫升(P&lt;0.05)。DON(100和250 ng/ml)增强了两种病原体对所有四种介质的诱导作用;观察到的反应显著高于预测的相加反应(P&lt;0.05)。SG(2和5 ng/ml)可显著增强李斯特菌和沙门氏菌对IL-1β和TNF-α的诱导作用(P&lt;0.05)。这些结果表明,在被镰刀菌污染的食物中遇到DON,在被水苏污染的室内环境中遇到SG,可以放大对食源性细菌病原体的先天炎症反应。
Health risks from microbial pathogens and toxins encountered in food and the environment continue to be of worldwide concern. The purpose of this research was to test the hypothesis that trichothecene mycotoxins amplify inflammatory responses to foodborne bacterial pathogens. We assessed the capacity of deoxynivalenol (DON) and satratoxin G (SG) to potentiate chemokine and proinflammatory cytokine production in RAW 264.7 murine macrophages induced by Listeria monocytogenes and Salmonella Typhimurium. When macrophage cultures were incubated with killed irradiated suspensions of the pathogens for 24 h, the minimum Listeria concentrations for induction of macrophage inhibitory protein 2 (MIP-2), interleukin-1beta (IL-beta), IL-6, and tumor necrosis factor alpha (TNF-alpha) were 0.01, 0.01, 1.0, and 1.0 microg/ml (P < 0.05) and the minimum Salmonella concentrations were 0.01, 0.01, 0.1, and 0.1 microg/ml, respectively (P < 0.05). Induction of all four mediators by both pathogens was potentiated by DON (at 100 and 250 ng/ml); observed responses were significantly higher than predicted additive responses (P < 0.05). SG (at 2 and 5 ng/ml) also significantly amplified induction of IL-1beta and TNF-alpha (P < 0.05) by both Listeria and Salmonella. These results indicate that DON encountered in Fusarium-contaminated food and SG from Stachybotrys-contaminated indoor environments could magnify innate inflammatory responses to foodborne bacterial pathogens.