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单核和空间转录学揭示了SAP诱导的肠损伤中的肠细胞异质性,分化和细胞通信机制

Lechang Zhang¹, Changqin Xu¹, Tong Su¹

¹Department of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.

Frontiers in immunology

|February 16, 2026

概括

严重的急性胰腺炎 (SAP) 通过改变细胞组成和空间组织而导致肠道损伤. 这项研究揭示了在SAP过程中脏中的免疫重新连接和干细胞功能受损,为再生机制提供了洞察力.

科学领域:

胃肠病学胃肠病学
分子生物学分子生物学
系统生物学系统生物学

背景情况:

严重的急性胰腺炎 (SAP) 是一种导致多器官损伤的关键状况,肠道损伤是严重的并发症.
驱动SAP诱导的肠损伤的精确机制,特别是关于细胞空间重组和功能相互作用的精确机制,仍然在很大程度上是未知的.

研究的目的:

在SAP诱导的肠损伤期间系统地分析肠道细胞组成,空间分布和功能的动态变化.
阐明严重急性胰腺炎的肠损伤背后的分子和空间机制.

主要方法:

构建严重急性胰腺炎 (SAP) 鼠标模型.
应用单核RNA测序 (snRNA-seq) 和空间转录组测序 (stRNA-seq) 进行综合分析.
将转录组数据与细胞通信和监管网络分析 (CellChat,SCENIC) 的整合.

主要成果:

SAP诱导了显著的内皮组织重塑,改变了包括干细胞,帕内斯细胞和免疫细胞在内的细胞群.
表皮细胞表现出转录转向免疫相互作用的转变,抗原呈现和抗菌基因的表达变化.
空间转录学揭示了细胞间通信的强化,特别是通过FN1信号轴,以及关键干细胞调节程序 (Hmga2 / Myb) 的活性降低.

结论:

严重的急性胰腺炎与空间有组织的乳腺重塑和上皮免疫重新连接有关.
改变的细胞间通信 (FN1轴) 和减弱的干细胞调控程序有助于SAP中的表皮再生受损.
这些发现为理解和潜在地治疗SAP诱导的肠损伤提供了一个空间信息的细胞框架.

关键词:

急性胰腺炎是什么?细胞通信的细胞通信.细胞异质性的细胞异质性肠道损伤是指肠道受伤.单核转录组学单核转录组学空间转录学空间转录学干细胞分化分化的干细胞.

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