慢性脏病患者肠道紧接口的表达变化:肠道透性的病原性机制
Georgia-Andriana Georgopoulou1, Marios Papasotiriou1, Pinelopi Bosgana2
1Division of Nephrology, Department of Internal Medicine, Medical School, University of Patras, 26504 Patras, Greece.
Biomedicines
|February 24, 2024
概括
慢性病 (CKD) 患者表现出肠道紧结蛋白,奥克卢丁和克劳丁-1. 这种肠道屏障功能障碍有助于增加CKD的内毒素和全身炎症.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 慢性病 (CKD) 中的全身炎症与肠道屏障功能障碍和肠道透性增加有关.
- 这种关联背后的机制尚未完全理解.
- 这项研究侧重于CKD患者的紧结结 (TJ) 蛋白.
研究的目的:
- 在CKD患者中调查肠道屏障参数.
- 为了评估紧结蛋白的表达,ocludin和claudin-1.
- 探索肠道屏障功能障碍,全身内毒素和炎症之间的关联.
主要方法:
- 从33名CKD患者 (I-IV期CKD或末期病[ESKD]) 和11个对照组的十二指肠活检.
- 组织学检查,针对奥克卢丁和克劳丁-1的免疫组织化学,针对内毒素的ELISA,以及针对细胞因子的流细胞计 (IL-1β,IL-6,IL-8,IL-10,TNF-α).
主要成果:
- 与对照组相比,CKD和ESKD患者的血清内毒素和IL-6,IL-8,IL-10水平升高.
- 在CKD患者中,肠道奥克卢丁和克劳丁-1表达显著下降.
- 减少的奥克卢丁和克劳丁-1表达与系统性内毒素症相反相关.
结论:
- 在CKD患者中,细胞表达奥克卢丁和克劳丁-1显著降低.
- 这种减少有助于全身性内毒毒症.
- 肠道屏障功能障碍在CKD的炎症反应中起作用.
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