Article(id=1321425574485144030, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1321425569611362746, articleNumber=null, orderNo=null, doi=10.20251/j.cnki.1003-3734.2026.07.002, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=1762099200000, acceptedDateStr=2025-11-03, onlineDate=1792982007856, onlineDateStr=2026-10-26, pubDate=1776182400000, pubDateStr=2026-04-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792982007856, onlineIssueDateStr=2026-10-26, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792982007856, creator=13701087609, updateTime=1792982007856, updator=13701087609, issue=Issue{id=1321425569611362746, tenantId=1146029695717560320, journalId=1235980733773295621, year='2026', volume='35', issue='7', pageStart='673', pageEnd='784', issueExtLink='null', onlineDate='null', pubDate='1776182400000', pubDateStr='2026-04-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1792982006695, creator='13701087609', updateTime=1792983136833, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1321430309837587328, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1321425569611362746, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1321430309837587329, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1321425569611362746, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=679, endPage=687, ext={EN=ArticleExt(id=1321425574720025055, articleId=1321425574485144030, tenantId=1146029695717560320, journalId=1235980733773295621, language=EN, title=Gastric organoids model reveals the host-pathogen interaction mechanism of Helicobacter pylori infection: from colonization mechanism to targeted therapy, columnId=null, journalTitle=Chinese Journal of New Drugs, columnName=null, runingTitle=null, highlight=null, articleAbstract=

Helicobacter pylori (H.pylori) gastric infection affects approximately 40% of the world's population and is a common cause of chronic gastritis and peptic ulcer, as well as a definite oncogenic factor in 89% of non-cardia gastric cancers. Preclinical research models, such as gastric tumor cell lines, gastric primary cell culture, and animal models of H.pylori infection, are difficult to simulate and cover the characteristics of chronic infection in the human stomach, hindering the elucidation of H.pylori infection pathogenesis. In recent years, with the breakthrough development of gastric organoid technology, the precise modeling of the H.pylori infection process within a three-dimensional human-derived microenvironment has become an important milestone in this field. This review duscusses the progress of gastric organoid platforms in studying the mechanisms of H.pylori infection, including bacterial colonization, host cell lineage-specific responses, the inflammation-to-carcinoma transformation mechanism, as well as target discovery and precison intervention strategies. These advances provide a basis for the eradication of H.pylori infection and the prevention of gastric cancer.

, authors=Shu-ting TIAN^{1, 2, 3}, Lin-li ZHANG^{1, 2, 3}, Yi-fang DENG^{1, 2, 3, *}, authorsList=Shu-ting TIAN, Lin-li ZHANG, Yi-fang DENG, authorCompany=null, correspAuthors=Yi-fang DENG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1321425574971683296, articleId=1321425574485144030, tenantId=1146029695717560320, journalId=1235980733773295621, language=CN, title=胃类器官模型揭示幽门螺杆菌感染的宿主-病原互作机制：从定植机制到靶向治疗, columnId=1236331162679955859, journalTitle=中国新药杂志, columnName=新药述评与论坛, runingTitle=null, highlight=null, articleAbstract=

幽门螺杆菌（Helicobacter pylori, H.pylori）胃部感染影响了全球约43%的人口，是慢性胃炎、消化性溃疡的常见诱因，也是90%非贲门部胃癌的明确致癌因子。临床前常用的研究模型如胃肿瘤细胞系、胃原代细胞培养、H.pylori感染动物模型，难以模拟、涵盖人胃慢性感染的特征，阻碍了H.pylori感染发病机制解析。近年来，随着胃类器官技术的突破性发展，通过三维人源微环境精准模拟H.pylori感染进程的实验，成为该领域的重要里程碑。本综述阐释了胃类器官平台在H.pylori感染机制中的进展，包括细菌定植、宿主细胞谱系特异性应答、炎-癌转化机制，以及靶点发现与精准干预策略研究，这些进展为根除H.pylori感染和胃癌预防提供依据。

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田书婷，女，硕士，研究方向：临床前药效学研究及机制研究、消化道类器官等。E-mail: m15928201363@163.com。

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田书婷，女，硕士，研究方向：临床前药效学研究及机制研究、消化道类器官等。E-mail: m15928201363@163.com。

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