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通过增强肠干细胞功能,Wnt/β-catenin通路的激活在肠有机单层中赋予了富蒙尼辛B1的耐受性
Shuai Zhang1, Yanan Cao1, Yiyi Shan1
1College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Animals : an open access journal from MDPI
|October 16, 2025
概括
禽类通过Wnt/β-catenin通路增强肠道干细胞功能,抵抗富蒙尼辛B1 (FB1) 菌毒素. 这促进了上皮的再生,增加了耐药性,降低了对毒素的敏感性.
科学领域:
- 兽医科学 兽医科学 兽医科学
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 富蒙尼辛B1 (FB1) 是一种在成的谷物中发现的有毒真菌毒素,对牲畜和食品安全构成风险.
- 禽类对FB1的敏感性较低,但这种耐受性的机制尚不清楚.
- 现有的3D有机体模型不允许直接研究FB1-肠上皮相互作用.
研究的目的:
- 建立并使用2D肠有机体单层模型来研究家禽对FB1的抵抗机制.
- 为了比较FB1在和猪肠道上皮细胞模型中的影响.
- 阐明参与家禽FB1耐受性的细胞和分子途径.
主要方法:
- 从特定无病原体的胚胎密室中开发2D肠器官单层模型.
- 和猪肠上皮模型暴露于FB1.
- 评估横体电阻,紧结基因表达和炎症性细胞因子水平.
- 对Wnt/β-catenin信号通路激活的分析,以应对FB1.
主要成果:
- 肠有机单层在FB1暴露后没有显著降低体电阻或紧结基因表达.
- 在模型中,FB1并没有导致炎症因子水平的显著波动.
- 暴露于FB1激活了肠干细胞中的Wnt/β-catenin通路,促进了上皮的再生.
结论:
- 2D肠器官模型有效模拟家禽-FB1相互作用,揭示了耐受性机制.
- 禽类对FB1的耐药性是由增强的肠干细胞功能和Wnt/β-catenin通路激活的介导,导致上皮细胞再生的增加.
- 向肠道干细胞功能为改善家禽FB1耐受性和减轻真菌毒素风险提供了一个新的策略.
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