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在人类肠道上皮细胞模型中,Lactobacillus murinus诱导CYP1A1表达并调节TNF-α诱导的反应

Husnain Ahmed^1,2, Azam A Sher^1,2, Julia A Bell^1,3,4

¹Comparative Enteric Diseases Laboratory, Michigan State University, East Lansing, MI 48824, USA.

International journal of molecular sciences

|December 11, 2025

概括

牛乳杆菌 (Lactobacillus murinus) 可能通过激活烯碳水化合物受体 (AHR) 来减少肠道炎症. 这种益生菌通过改善肠道屏障功能,显示出治疗炎症性肠病 (IBD) 的潜力.

科学领域:

胃肠病学胃肠病学
免疫学免疫学免疫学
微生物学微生物学

背景情况:

抗瘤坏死因子α (TNF-α) 疗法对于炎症性肠病 (IBD) 是常见的,但它们的有效性随着时间的推移而变化,并且往往会降低.
由于当前IBD治疗的局限性,需要新的治疗方法.

研究的目的:

为了调查Lactobacillus murinus (L. murinus) 是否可以降低TNF-α诱导的炎症反应在人肠道结肠炎的体外模型.
探索基碳化合物受体 (AHR) 在调解L. murinus.效应中的作用.

主要方法:

使用使用TNF-α刺激的Caco-2肠道细胞创建了体外结肠炎模型.
细胞先用L. murinus或AHR配体进行预处理.
评估了对AHR激活,屏障完整性 (通过TEER测量) 和IL-8分泌的影响.
测量了AHR位基因的CYP1A1mRNA表达,作为AHR调节的标志物.

主要成果:

TNF-α显著损害了表皮屏障功能,增加了IL-8分泌.
在L. murinus的治疗前,增加了CYP1A1的表达,并减弱了TNF-α诱导的屏障损伤和IL-8释放.
合成的AHR配体没有复制L. murinus的保护作用,表明配体特异性的AHR反应.

结论:

L. murinus可能通过AHR信号减轻TNF-α诱导的肠道炎症和屏障功能障碍.
这项研究突出了IBD治疗的潜在益生菌机制.
需要进一步的研究来确认AHR的依赖性,并确定涉及的特定L. murinus代谢物.

关键词:

CYP1A1的表达方式.牛乳杆菌 (Lactobacillus murinus) 是一种植物.亚利碳化合物受体是什么肠道炎症是一种肠道炎症.

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