杆菌诱导的炎症性癌症转化微环境驱动胃癌的发生
Yufei Fu1, Jiajing Tong2, Manxuan Zhu1
1Key Laboratory of Digestive Pathophysiology of Zhejiang Province, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China.
Cellular and molecular gastroenterology and hepatology
|February 27, 2026
概括
杆菌 (H. pylori) 感染即使在根除之后也会造成持续的炎症微环境,导致胃癌. 特定的癌症相关纤维细胞 (CAF) 亚型是这种恶性转变和免疫抑制的关键驱动因素.
科学领域:
- 胃肠病学 胃肠病学
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
背景情况:
- 根除Helicobacter pylori (H. pylori) 可以降低胃癌的风险,但对晚期缩性胃炎的影响有限.
- 在H. pylori根除后,持续的炎症癌变微环境 (ICTM) 驱动胃癌发生.
研究的目的:
- 调查H. pylori感染和根除对ICTM的影响.
- 为了确定细胞参与者和驱动胃癌发生后根除的机制.
主要方法:
- 从正常患者,H. pylori感染者和根除后患者的胃粘膜单细胞RNA测序.
- 使用多重免疫光和初级癌症相关纤维细胞 (CAF) 实验进行验证.
主要成果:
- 杆菌感染深刻地改变了ICTM,在根除后具有明显的上皮细胞轨迹.
- 免疫调节CAFs (iCAFs),特别是CCN2+ iCAF1和C3+ iCAF3,促进上皮质恶性瘤和免疫抑制.
- 杆菌感染重新编程iCAFs,诱导细胞外矩阵重组,衰老,并促进表皮质恶性转变和干性.
结论:
- H. pylori 感染建立了一个持续的 ICTM 根除后,有助于胃癌发生.
- 感染驱动的iCAF分化对于上皮质恶性转变和免疫抑制至关重要.
- 针对特定的iCAF亚型为后期H. pylori根除疗法提供了一个有希望的治疗策略.
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