Helicobacter pylori Eradication Is Associated With a Reduced Risk of Metachronous Gastric Neoplasia by Restoring Immune Function in the Gastric Mucosa

IF 4.3 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter Pub Date : 2025-04-01 DOI:10.1111/hel.70030

Min-Jae Kim, Yeonjin Je, Jaeyoung Chun, Young Hoon Youn, Hyojin Park, Ji Hae Nahm, Jie-Hyun Kim

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Abstract

Background

Helicobacter pylori infection is a significant contributing factor of gastric cancer. Metachronous neoplasms also pose a risk. The mechanism underlying the impact of H. pylori eradication on preventing metachronous gastric cancer is unclear. This study aimed to investigate immunity changes in gastric mucosa after H. pylori eradication and to identify mechanisms preventing metachronous recurrence.

Materials and Methods

Patients diagnosed with gastric neoplasm and H. pylori infection, who underwent endoscopic resection, were included. Thirty-six cases of metachronous neoplasms occurring after eradication (metachronous group) were compared to 36 controls matched for age, sex, atrophy, and metaplasia (control group). Histological features and immunohistochemical staining for T-cell (CD3, CD4, and CD8) and immune exhaustion (forkhead/winged helix transcription factor and programmed cell death-ligand 1) markers in the non-tumor-bearing mucosa were evaluated.

Results

In histologic features, glandular atrophy and intestinal metaplasia in the gastric mucosa significantly improved following H. pylori eradication in the control group (p < 0.001, 0.008), whereas they did not improve in the metachronous group (p = 0.449, 0.609). CD8 and CD8/CD3 ratios increased in the control group (p < 0.001, 0.04), but did not show differences in the metachronous group (p = 0.057, 0.245). The CD4/CD3 ratio and programmed cell death-ligand 1/CD4 expression significantly decreased after H. pylori eradication in the control group (p = 0.003, 0.042), but not in the metachronous group (p = 0.54, 0.55).

Conclusions

This observational study suggests that H. pylori eradication may prevent the recurrence of gastric neoplasia by improving histological inflammation and overcoming immune exhaustion.

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通过恢复胃黏膜免疫功能，根除幽门螺杆菌与降低异时性胃肿瘤的风险相关

背景幽门螺杆菌感染是胃癌发生的重要因素。异时性肿瘤也有风险。根除幽门螺杆菌对预防异时性胃癌的作用机制尚不清楚。本研究旨在探讨幽门螺杆菌根除后胃黏膜的免疫变化，并确定预防异时性复发的机制。材料与方法对经内镜切除的胃肿瘤合并幽门螺杆菌感染患者进行研究。将36例根除后发生的异时性肿瘤（异时性组）与36例年龄、性别、萎缩和化生相匹配的对照组（对照组）进行比较。评估非荷瘤粘膜t细胞（CD3、CD4和CD8）和免疫衰竭（叉头/翼螺旋转录因子和程序性细胞死亡配体1）标志物的组织学特征和免疫组化染色。结果在组织学特征上，对照组幽门螺杆菌根除后胃粘膜腺萎缩和肠化生明显改善（p < 0.001, 0.008），而异时性组无明显改善（p = 0.449, 0.609）。对照组CD8和CD8/CD3比值升高（p < 0.001, 0.04），而异时组无差异（p = 0.057, 0.245）。对照组幽门螺杆菌根除后CD4/CD3比值和程序性细胞死亡配体1/CD4表达显著降低（p = 0.003, 0.042），而异时性组无显著降低（p = 0.54, 0.55）。结论本观察性研究提示幽门螺杆菌的根除可能通过改善组织学炎症和克服免疫衰竭来预防胃肿瘤的复发。

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来源期刊

Helicobacter 医学-微生物学

CiteScore

8.40

自引率

9.10%

发文量

审稿时长

2 months

期刊介绍： Helicobacter is edited by Professor David Y Graham. The editorial and peer review process is an independent process. Whenever there is a conflict of interest, the editor and editorial board will declare their interests and affiliations. Helicobacter recognises the critical role that has been established for Helicobacter pylori in peptic ulcer, gastric adenocarcinoma, and primary gastric lymphoma. As new helicobacter species are now regularly being discovered, Helicobacter covers the entire range of helicobacter research, increasing communication among the fields of gastroenterology; microbiology; vaccine development; laboratory animal science.