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在反应性氧物种缺乏症中肠道O-葡萄糖的表征

Radka Saldova^1,2,3, Kristina A Thomsson⁴, Hayden Wilkinson^1,2,3

¹National Institute for Bioprocessing, NIBRT GlycoScience Group, Research and Training, Blackrock, Dublin, Ireland.

|March 14, 2024

概括

NADPH氧化酶 (NOX) 活动影响肠道粘液O-糖体. 在小鼠中的遗传NOX无活化改变了这些甘氨酸,可能导致炎症性肠病 (IBD) 和肠道失活症.

科学领域:

胃肠病学胃肠病学
免疫学免疫学免疫学
葡萄糖生物学葡萄糖生物学

背景情况:

炎症性肠病 (IBD) 涉及与宿主遗传和肠道微生物相关的慢性肠道炎症.
NADPH氧化酶 (NOX) 产生反应性氧物种 (ROS),这对抗微生物防御,氧化还原信号和肠道屏障完整性至关重要.
氧化无活化和随后的粘液层破坏与IBD病原发生有关.

研究的目的:

为了研究ROS依赖性修饰对上皮质糖化酶的影响.
在具有遗传NOX无活化 (Cyba突变) 的小鼠中分析结肠和乳腺粘素O-糖体.

主要方法:

分析了来自结肠和大肠组织的纯化小鼠粘膜.
使用水友相互作用超高性能液体染色学 (HILIC-UPLC) 释放和表征了O-甘氨酸.
使用外甘油酶消化和质谱仪进行了详细的糖分析.

主要成果:

在Cyba突变小鼠的皮质中发现了五种新型甘氨酸.
在结肠和大肠中观察到O-甘氨酸的轻微变化.
具体的变化包括结肠中Fuc-Gal增加的终端HexNAc和核心2甘氨酸,结肠中的核心3甘氨酸减少,化增加,以及大肠中的硫化减少.

结论:

NADPH氧化酶活性显著影响肠道粘素O-甘氨酸组成.
这些O-甘氨酸的变化可能在肠道失调和IBD特征的慢性炎症的发展中发挥作用.

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