乳杆菌delbrueckii表面蛋白P4430通过调节巨细胞两极分化通过Mincle减轻肠道炎症
Xiangyu Zhang1, Xiangyi Zeng2, Yujun Wu2
1State Key Laboratory of Animal Nutrition and Feeding, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China; Frontier Science Center of Molecular Design Breeding, Ministry of Education, Beijing 100193, China.
Cell reports
|January 22, 2026
概括
乳酸菌delbrueckii,通常在性结肠炎 (UC) 中减少,其表面蛋白质P4430,可以减少肠道炎症. 通过准Mincle,P4430抑制了巨细胞的炎症反应,提供了潜在的UC疗法.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
背景情况:
- 性结肠炎 (UC) 涉及肠道炎症,屏障问题和失生症,治疗方法很少.
- 在低出生体重小猪,DSS诱导性大肠炎模型和UC患者中观察到低水平的Lactobacillus delbrueckii.
研究的目的:
- 调查乳酸菌delbrueckii及其表面蛋白在减轻肠道炎症中的作用.
- 确定具有UC治疗潜力的特定细菌成分.
主要方法:
- 在不同的结肠炎模型和人类UC患者中对L. delbrueckii丰度的比较分析.
- 对L.delbrueckii及其表面蛋白对巨细胞的抗炎作用的评估.
- 关键表面蛋白P4430及其作用机制的识别和表征,包括Mincle相互作用.
主要成果:
- L. delbrueckii及其表面蛋白质显著降低了肠道炎症.
- 表面蛋白质P4430被确定为一个关键因素,抑制M1巨细胞极化和炎症反应.
- P4430通过结合和抑制C型乳素受体而起作用.
结论:
- L.delbrueckii及其表面蛋白P4430显示出对性结肠炎的显著治疗潜力.
- P4430的机制包括抑制Mincle,从而调节巨细胞的炎症途径.
- 连体细菌及其组成部分代表了治疗UC等肠道炎症疾病的有希望的途径.
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