长期鼻炎与鼻多的上皮mTORC1活性增加
George X Huang1,2, Nils R Hallen1,2, Minkyu Lee1,2
1Jeff and Penny Vinik Center for Translational Immunology Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital; Boston, MA.
bioRxiv : the preprint server for biology
|October 31, 2023
概括
空气道上皮细胞使用一种涉及mTORC1的代谢途径,在喘和CRSwNP等慢性呼吸道疾病中驱动炎症. 这种新陈代谢重编程与疾病严重程度和特定的炎症概况有关.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢途径 代谢途径
- 皮质细胞生物学 皮质细胞生物学
背景情况:
- 呼吸道上皮在慢性呼吸道疾病中至关重要.
- 表皮细胞驱动炎症的机制尚未完全理解.
研究的目的:
- 定义表皮细胞驱动炎症的机制.
- 为了研究呼吸道上皮细胞的转录形状.
主要方法:
- 对排序的气道上皮细胞 (EpCs) 的转录基因分析.
- 使用了批量和单细胞RNA测序 (scRNA-seq).
- 使用免疫光和ex vivo功能测定验证的结果.
主要成果:
- 具有鼻息肉的慢性鼻炎 (CRSwNP) EpCs显示了增强的糖解.
- 猛素复合体1 (mTORC1) 的哺乳动物标调节了这种糖分分解程序.
- mTORC1的活动对EPC细胞因子的产生至关重要 (例如,CXCL8,IL-33).
- 糖解活性与CRSwNP和喘中的T2炎症相关.
结论:
- 代谢轴在慢性呼吸道炎症中支持表皮细胞因子生成.
- 这个轴在CRSwNP和喘中促进T2和非T2炎症.
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