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S1P/S1PR3轴驱动了长期鼻炎与鼻的上皮功能障碍和2型炎症
Han Chen1, Lin Wang1, Lin Han2
1Department of Otolaryngology Head and Neck Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China; Shandong Provincial Engineering Research Center for Precision Diagnosis and Therapy in Otorhinolaryngology, Qingdao, Shandong, China; Qingdao Municipal Key Laboratory of Nasal Diseases, Qingdao, Shandong, China.
斯芬戈辛-1-酸盐 (S1P) /S1P受体 (S1PR) 轴,特别是S1PR3,驱动长表皮功能障碍和慢性鼻炎与鼻 (CRSwNP) 的2型炎症. 针对这一轴可能为CRSwNP提供新的治疗方法和生物标志物.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 带鼻息肉的慢性鼻炎 (CRSwNP) 涉及表皮屏障缺陷和2型炎症,但上游调节者尚不清楚.
- 乙性CRSwNP (EOS CRSwNP) 的生物标志物有限,阻碍了有效的疾病分层.
研究的目的:
- 调查基-1-酸盐 (S1P) /S1P受体 (S1PR) 轴在CRSwNP病变发生中的作用.
- 评估S1P/S1PR轴作为EOS CRSwNP的潜在辅助生物标志物.
主要方法:
- 在血清和鼻腔组织中测量S1P水平.
- 在实验室中利用人类鼻上皮细胞模型研究S1P/S1PR3对上皮屏障功能和上皮-介质细胞过渡 (EMT) 的影响.
- 采用了转录基因分析,多重免疫光学和具有S1PR3抑制的小鼠CRSwNP模型.
主要成果:
- 在CRSwNP患者中S1P水平升高,与疾病严重程度和EMT标志物相关,特别是在EOS CRSwNP中.
- 在人类鼻上皮细胞中,S1P诱导了EMT和通过S1PR3损害了屏障功能.
- 在小鼠模型中S1PR3的抑制减少了聚的形成,炎症和Th2细胞因子.
- 血清S1P与乙氨基酸百分比相结合,改善了EOS CRSwNP的诊断性能.
结论:
- 在CRSwNP中,S1P/S1PR3轴是表皮功能障碍和2型炎症之间的关键联系.
- S1PR3代表了CRSwNP的一个潜在的治疗点.
- S1P/S1PR轴显示出作为CRSwNP患者分层的辅助生物标志物的前景.
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