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细菌花CwpFM通过氧化应激和NLRP3 / NF-κB通路诱导结肠组织损伤和炎症反应

Qiang Shan¹, Xue Wang¹, Hao Yang¹

¹Department of Veterinary Clinical Sciences, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; Sanya Institute of China Agricultural University, Sanya 572025, China.

The Science of the total environment

|May 12, 2024

概括

细菌大麦肠毒素CwpFM通过诱导氧化应激和激活NLRP3 / NF-κB信号来引起肠道炎症,同时抑制抗氧化途径. 这项研究提供了对食品安全和潜在治疗点的见解.

科学领域:

微生物学微生物学
免疫学免疫学免疫学
毒理学毒理学毒理学

背景情况:

牛奶中的Bacillus cereus (B. cereus) 是一个公共卫生问题,导致食物中毒.
B. cereus 肠毒素有助于胃肠道疾病.

研究的目的:

研究B. cereus肠毒素CwpFM在氧化应激和炎症中的作用.
阐明CwpFM引起的肠损伤背后的分子机制.

主要方法:

对暴露于CwpFM.FM的小鼠结肠的蛋白质组分析.
使用Caco-2细胞进行体外研究以评估细胞毒性,ROS积累和信号通路激活 (NLRP3 / NF-κB,NFE2L2 / HO-1).
使用ROS抑制剂 (NAC),NFE2L2激活剂 (NK-252),NF-κB抑制剂 (ADPC) 和NLRP3抑制剂 (MCC950) 的药理干预.

主要成果:

CwpFM诱导了结肠细胞中的氧化应激,炎症和细胞毒性.
CwpFM激活了NLRP3 / NF-κB通路并抑制了抗氧化剂NFE2L2 / HO-1信号传递.
抑制ROS,激活NFE2L2或阻断NLRP3 / NF-κB通路可以减轻CwpFM引起的炎症.

结论:

通过氧化应激和NLRP3/NF-κB激活,CwpFM触发肠道炎症,部分通过抑制NFE2L2/HO-1信号传递.
了解这些机制对于开发B. cereus食物传播疾病的诊断和治疗至关重要.

关键词:

细菌花的花类植物.在CwpFMFM中.进入毒素 (enterotoxin) 是一种有毒的物质.在NFE2L2中,NFE2L2是NFE2L2 在NLRP3/NF-κB中使用.有反应性氧物种的反应性氧物种.

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