DYSREGULATION OF IGA PRODUCTION AND IGA NEPHROPATHY INDUCED BY THE TRICHOTHECENE VOMITOXIN
DYSREGULATION OF IGA PRODUCTION AND IGA NEPHROPATHY INDUCED BY THE TRICHOTHECENE VOMITOXIN
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DOI：
10.1016/0278-6915(89)90141-5
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发表时间：
1989-06-01
影响因子：
4.3
通讯作者：
WARNER, RL
中科院分区：
文献类型：
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作者：
PESTKA, JJ;MOORMAN, MA;WARNER, RL
在B6C3F1小鼠中评价了呕吐毒素饮食暴露对血清免疫球蛋白A（伊加）的影响。与喂食2、10或50 ppm呕吐毒素的小鼠相比，喂食25 ppm呕吐毒素的小鼠血清伊加水平最大程度升高。显著增加后检测到的小鼠喂养25 ppm的呕吐毒素，和伊加水平增加超过17倍后，24周的毒素暴露。在呕吐毒素治疗期间，血清伊加也表现出从主要是单体伊加到主要是聚合伊加的显著转变。血清IgG和IgM降低治疗小鼠，表明该效果是同种型特异性的。升高的血清伊加没有观察到在小鼠中，当对照饮食喂养的水平相当于呕吐毒素处理的小鼠，表现出拒食消耗。伊加生产显着增加自发和有丝分裂原刺激的脾细胞培养暴露于呕吐毒素的小鼠相比，从即兴准备的文化。或进料限制控制。免疫荧光染色显示肾小球系伊加和电子显微镜显示电子致密沉积物中的呕吐毒素治疗小鼠的肾小球，但在对照组中没有。本研究中观察到的伊加产生和肾小球伊加积累的失调与人类伊加肾病（全球最常见的肾小球肾炎形式）的特征高度相似。
The effect of dietary exposure to vomitoxin on serum immunoglobulin A (IgA) was evaluated in the B6C3F1 mouse. Levels of serum IgA were elevated maximally in mice fed 25 ppm vomitoxin in comparison with levels in mice fed 2, 10 or 50 ppm vomitoxin. Significant increases were detectable after as few as 4 wk in mice fed 25 ppm vomitoxin, and IgA levels were increased more than 17-fold after 24 wk of toxin exposure. Serum IgA also exhibited a marked shift from primarily monomeric IgA to primarily polymeric IgA during vomitoxin treatment. Serum IgG and IgM decreased in treated mice, suggesting that the effect was isotype-specific. Elevated serum IgA was not observed in mice when control diet was fed at levels equivalent to those consumed by vomitoxin-treated mice, which exhibited feed refusal. IgA production was significantly increased in both spontaneous and mitogen-stimulated splenocyte cultures from mice exposed to vomitoxin in comparison with cultures prepared from ad lib. or feed-restricted controls. Immunofluorescence staining revealed marked accumulation of mesangial IgA and electron mciroscopy showed electron-dense deposits in the glomeruli of vomitoxin-treated mice but not in those of controls. Dysregulation of IgA production and accumulation of glomerular IgA as observed in this study were highly analogous to the characterisrtics of human IgA mephropathy, the most common form of glomerulonephritis worldwide.