在Helicobacter pylori感染和自身免疫性胃炎中揭示与癌症相关的转化性细胞
Stella G Hoft1, Michelle Brennan2, Javier A Carrero1
1Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, Missouri.
Gastroenterology
|September 5, 2024
概括
无论是Helicobacter pylori (Hp) 感染还是自身免疫性胃炎 (AIG),都会导致转质形成,并具有类似的癌症风险. 发现了一种表达ANPEP/CD13的共享癌症状转化细胞,有助于早期检测胃癌风险.
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:
- 慢性炎症,包括Helicobacter pylori (Hp) 感染和自身免疫性胃炎 (AIG),可能导致胃代谢.
- 胃代谢是胃癌发展的已知危险因素.
- 了解从HP感染到AIG的转质形成的区别对于评估癌症风险至关重要.
研究的目的:
- 为了调查和比较由HP感染和AIG引起的转质形成.
- 在这两种条件下,描述元塑性细胞的分子特征.
- 为了识别潜在的癌症相关的生物标志物在metaplastic细胞.
主要方法:
- 利用小鼠模型和人类参与者进行比较分析.
- 进行了胃病理和转化成形的组织病理学评估.
- 采用单细胞转录学来定义超塑性细胞的分子特征.
- 通过免疫光检测证实了生物标志物的表达.
主要成果:
- 在HP感染和AIG之间,转化形质的基因病理和转录形状是可比的.
- 根据炎症背景,鉴定出多种多样的转移性亚型,存在微妙的患病率差异.
- 发现了一种类似癌症的转化性亚型,类似于不完全的肠道转化,在Hp和AIG中表达ANPEP/CD13.
- 肝炎感染并没有诱导独特的超塑性细胞表型.
结论:
- 无论是HP感染还是AIG都会诱导多种类型的超塑性细胞.
- 在这两种情况中,鉴定出与癌症相关的转移性细胞 (ANPEP/CD13+) 凸显了它们的致癌潜力.
- 这一发现可以为慢性胃炎患者的早期检测策略和风险分层提供信息.
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