NOX2调解NLRP3 / ROS,促进慢性鼻炎的鼻膜上皮质炎症与鼻
Sijie Jiang1,2,3,4, Benjian Zhang1,2,3,4, Sihui Wen1,2,3,4
1Department of Otolaryngology Head and Neck Surgery, Xiangya Hospital of Central South University, Changsha, China.
Heliyon
|September 27, 2024
概括
氧化应激和NLRP3炎症酶激活在具有鼻息肉的慢性鼻炎 (CRSwNP) 中增加. NOX2是这些过程的关键调节者,这表明它是CRSwNP的潜在治疗标.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 分子医学是分子医学.
背景情况:
- 氧化应激在鼻腔粘膜炎症中起到有限的作用.
- 带鼻息肉的慢性鼻炎 (CRSwNP) 涉及复杂的炎症途径.
- 在CRSwNP上皮细胞中氧化应激的特定机制需要进一步阐明.
研究的目的:
- 为了研究氧化应激在CRSwNP上皮细胞中的作用.
- 阐明CRSwNP中氧化应激和炎症酶激活的机制.
- 为了确定CRSwNP.的潜在治疗点.
主要方法:
- 在CRSwNP上皮细胞的单细胞RNA测序 (scRNA-seq).
- 氧化应激,炎症酶激活和NOX家族表达的分析.
- 使用siRNA,等离子体转染和特定诱导剂/抑制剂 (TMAO,MCC950) 的体外功能研究.
- 活性氧物种 (ROS) 和NOX2定位的可视化.
主要成果:
- scRNA-seq数据显示,CRSwNP上皮细胞中氧化应激增加和NLRP3炎症组分数增加.
- 在体外,脂聚糖诱导了ROS,NLRP3炎症酶激活,以及上皮细胞警示蛋白表达.
- 在CRSwNP上皮细胞中,增加的NOX2表达与增加的ROS,NLRP3炎症酶激活和警报蛋白表达相关.
- 通过siRNA抑制NOX2减少了这些影响,而MCC950抑制了警报蛋白的表达.
结论:
- 在CRSwNP中,NOX2是ROS积累和NLRP3炎症酶激活的关键调节者.
- 向NOX2为CRSwNP提供了一个有前途的治疗策略.
- 了解氧化应激和炎症酶通路之间的相互作用是CRSwNP治疗的关键.
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