具有trx1高表达的Helicobacter pylori通过上调IL23A/NF-κB/IL8通路促进胃疾病
Xin Guan1, Jing Ning1, Weiwei Fu1
1Beijing Key Laboratory for Helicobacter pylori Infection and Upper Gastrointestinal Diseases, Department of Gastroenterology, Peking University Third Hospital, Beijing, China.
Helicobacter
|April 30, 2024
概括
杆菌的 thioredoxin-1 (Trx1) 和 arginase (RocF) 是致病性的关键,可以选高度致病性菌株. Trx1增强了细菌的粘附性,并通过NF-κB通路促进胃病.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 在瘤学瘤学.
背景情况:
- 杆菌感染是胃癌的主要原因.
- 铁素-1 (Trx1) 和氨酶 (RocF) 是 H. pylori 的毒性因子.
- 对于Trx1和RocF用于查的临床效用以及高Trx1表达的致病性尚不清楚.
研究的目的:
- 评估H. pylori Trx1和RocF作为用于查高度致病性H. pylori的生物标志物.
- 阐明高Trx1表达的H. pylori菌株的致病机制.
主要方法:
- 定量实时PCR (RT-qPCR) 用于测量胃组织中的H. pylori trx1和rocF表达.
- RNA测序 (RNA-seq) 用于分析与H. pylori共同培养的GES-1细胞中的基因表达.
- 使用RT-qPCR,ELISA,西斑,免疫组织化学和免疫光学验证差异表达的基因和途径.
- 对细菌粘附于GES-1细胞的评估.
主要成果:
- 与胃炎相比,H. pylori trx1和rocF表达在胃癌和胃潰瘍群中显著高.
- 对H. pylori trx1和rocF的联合诊断显示了对查的高度敏感性.
- 高Trx1表达的H. pylori表现出对GES-1细胞的增强粘附.
- 观察到IL-23A/NF-κB/IL17A,IL6和IL8通路的升调.
结论:
- 杆菌Trx1和RocF作为有价值的生物标志物用于临床查高度致病性杆菌和预测感染结果.
- 在H. pylori中高Trx1表达增强了细菌的粘附性,并通过激活NF-κB信号通路来促进胃疾病的发展.
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