Helicobacter最新文献

{"title":"Artificial Intelligence in Endoscopy for Predicting Helicobacter pylori Infection: A Systematic Review and Meta-Analysis","authors":"Yiwen Jiang,&nbsp;Hengxu Yan,&nbsp;Jiatong Cui,&nbsp;Kaiqiang Yang,&nbsp;Yue An","doi":"10.1111/hel.70026","DOIUrl":"10.1111/hel.70026","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>This meta-analysis aimed to assess the diagnostic performance of artificial intelligence (AI) based on endoscopy for detecting <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A comprehensive literature search was conducted across PubMed, Embase, and Web of Science to identify relevant studies published up to January 10, 2025. The selected studies focused on the diagnostic accuracy of AI in detecting <i>H. pylori</i>. A bivariate random-effects model was employed to calculate pooled sensitivity and specificity, both presented with 95% confidence intervals (CIs). Study heterogeneity was assessed using the <i>I</i>² statistic.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of 604 studies identified, 16 studies (25,002 images or patients) were included. For the internal validation set, the pooled sensitivity, specificity, and area under the curve (AUC) for detecting <i>H. pylori</i> were 0.91 (95% CI: 0.84–0.95), 0.91 (95% CI: 0.86–0.94), and 0.96 (95% CI: 0.94–0.97), respectively. For the external validation set, the pooled sensitivity, specificity, and AUC were 0.91 (95% CI: 0.86–0.95), 0.94 (95% CI: 0.90–0.97), and 0.98 (95% CI: 0.96–0.99). For junior clinicians, the pooled sensitivity, specificity, and AUC were 0.76 (95% CI: 0.66–0.83), 0.75 (95% CI: 0.70–0.80), and 0.81 (95% CI: 0.77–0.84). For senior clinicians, the pooled sensitivity, specificity, and AUC were 0.81 (95% CI: 0.74–0.86), 0.89 (95% CI: 0.86–0.91), and 0.92 (95% CI: 0.90–0.94).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Endoscopy-based AI demonstrates higher diagnostic performance compared to both junior and senior endoscopists. However, the high heterogeneity among studies limits the strength of these findings, and further research with external validation datasets is necessary to confirm the results.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 2","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter to the Editor: “Efficacy of Lactobacillus spp. Supplementation in Helicobacter pylori Eradication: A Systematic Meta-Analysis of Randomized Controlled Trials With Trial Sequential Analysis”","authors":"Ben-Gang Zhou,&nbsp;Yao-Yao Li,&nbsp;Yan-Bing Ding","doi":"10.1111/hel.70027","DOIUrl":"10.1111/hel.70027","url":null,"abstract":"","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 2","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Innate Immunity in Helicobacter pylori Infection and Gastric Oncogenesis","authors":"Yuheng Zhang,&nbsp;Zhiyu Yan,&nbsp;Yuhao Jiao,&nbsp;Yunlu Feng,&nbsp;Shengyu Zhang,&nbsp;Aiming Yang","doi":"10.1111/hel.70015","DOIUrl":"https://doi.org/10.1111/hel.70015","url":null,"abstract":"<p><i>Helicobacter pylori</i> is an extremely common cause of gastritis that can lead to gastric adenocarcinoma over time. Approximately half of the world's population is infected with <i>H. pylori</i>, making gastric cancer the fourth leading cause of cancer-related deaths worldwide. Innate immunity significantly contributes to systemic and local immune responses, maintains homeostasis, and serves as the vital link to adaptive immunity, and in doing so, mediates <i>H. pylori</i> infection outcomes and consequent cancer risk and development. The gastric innate immune system, composed of gastric epithelial and myeloid cells, is uniquely challenged by its need to interact simultaneously and precisely with commensal microbiota, exogenous pathogens, ingested substances, and endogenous exfoliated cells. Additionally, innate immunity can be detrimental by promoting chronic infection and fibrosis, creating an environment conducive to tumor development. This review summarizes and discusses the complex role of innate immunity in <i>H. pylori</i> infection and subsequent gastric oncogenesis, and in doing so, provides insights into how these pathways can be exploited to improve prevention and treatment.</p>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 2","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.70015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143639027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flagellar Assembly Factor FliW2 De-Represses Helicobacter pylori FlaA-Mediated Motility by Allosteric Obstruction of Global Regulator CsrA","authors":"Marcia Shu-Wei Su,&nbsp;Benjamin Dickins,&nbsp;Fang Yie Kiang,&nbsp;Wei-Jiun Tsai,&nbsp;Yueh-Lin Chen,&nbsp;Jenn-Wei Chen,&nbsp;Shuying Wang,&nbsp;Pei-Jane Tsai,&nbsp;Jiunn-Jong Wu","doi":"10.1111/hel.70019","DOIUrl":"https://doi.org/10.1111/hel.70019","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p><i>Helicobacter pylori</i> colonizes the human stomach as a dominant member of the gastric microbiota and constitutively expresses flagellar motility for survival. Carbon storage regulator A (CsrA) is a posttranscriptional global regulator and a critical determinant of <i>H. pylori</i>'s motility and pathogenicity. The regulation of <i>H. pylori</i> CsrA is still uncertain although in other species CsrA is reported to be antagonized by small RNAs and proteins. In this study, we attempted to unveil how CsrA is regulated and hypothesized that <i>H. pylori</i> CsrA activity is antagonized by a flagellar assembly factor, FliW2, via protein allosteric obstruction.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>Multiple sequence comparisons indicated that, along its length and in contrast to <i>fliW1</i>, the <i>fliW2</i> of <i>H. pylori</i> J99 is conserved. We then generated an isogenic Δ<i>fliW2</i> strain whose function was characterized using phenotypic and biochemical approaches. We also applied a machine learning approach (AlphaFold2) to predict FliW2-CsrA binding domains and investigated the FliW2-CsrA interaction using pull-down assays and in vivo bacterial two-hybrid systems.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We observed the reduced expression of major flagellin FlaA and impaired flagellar filaments that attenuated the motility of the Δ<i>fliW2</i> strain. Furthermore, a direct interaction between FliW2 and CsrA was demonstrated, and a novel region of the C-terminal extension of CsrA was suggested to be crucial for CsrA interacting with FliW2. Based on our AlphaFold2 prediction, this C-terminal region of FliW2-CsrA interaction does not overlap with CsrA's N-terminal RNA binding domain, implying that FliW2 allosterically antagonizes CsrA activity and restricts CsrA's binding to <i>flaA</i> mRNAs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our data points to novel regulatory roles that the <i>H. pylori</i> flagellar assembly factor FliW2 has in obstructing CsrA activity, and thus FliW2 may indirectly antagonize CsrA's regulation of <i>flaA</i> mRNA processing and translation. Our findings reveal a new regulatory mechanism of flagellar motility in <i>H. pylori</i>.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 2","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.70019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143602475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Helicobacter pylori and Colorectal Cancer: Meeting Sir Austin Bradford Hill's Causality Criteria","authors":"Juan Sebastián Frías-Ordoñez,&nbsp;Arnoldo Riquelme,&nbsp;Hernando Marulanda-Fernandez,&nbsp;Lina Otero-Parra,&nbsp;José Augusto Urrego,&nbsp;Elder Otero-Ramos,&nbsp;José Darío Portillo-Miño,&nbsp;William Otero Regino","doi":"10.1111/hel.70024","DOIUrl":"https://doi.org/10.1111/hel.70024","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Epidemiological and experimental studies have suggested that chronic <i>H. pylori</i> infection may be associated with colorectal cancer (CRC), a topic of growing interest. The Bradford-Hill criteria are the mainstay of the epidemiological approach to causal inference. We aim to evaluate the epidemiological evidence based on the Bradford-Hill causality criteria and the association between <i>H. pylori</i> and CRC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methodology</h3>\u0000 \u0000 <p>A literature review of the databases search: Pubmed, ScienceDirect, Embase, SciELO, Cochrane, and Medline. There are no limits in a period. Information sources that were coherent with the objectives set were selected.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Applying the Bradford Hill criteria, we can conclude that <i>H. pylori</i> is positively associated with CRC. The current epidemiological findings should stimulate future studies to explain how <i>H. pylori</i> interacts with intestinal dysbiosis and the role of <i>H. pylori</i> eradication in the treatment and prevention of CRC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p><i>H. pylori</i> reasonably meets the Bradford Hill criteria for causality. Further studies are required to consolidate the data and generate strategies to determine whether <i>H. pylori</i> eradication translates into decreased CRC incidence and mortality in large populations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 2","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global Population Structure, Virulence Factors and Antibiotic Resistance of Helicobacter pylori: A Pooled Analysis of 4067 Isolates From 76 Countries","authors":"Mengyi Zhu,&nbsp;Xianfeng Xu,&nbsp;Pengpeng Cai,&nbsp;Tianpei Wang,&nbsp;Meng Zhu,&nbsp;Caiwang Yan,&nbsp;Qianglong Pan,&nbsp;Chen Chen,&nbsp;Ying Wu,&nbsp;Guoxin Zhang,&nbsp;Guangfu Jin","doi":"10.1111/hel.70025","DOIUrl":"https://doi.org/10.1111/hel.70025","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;&lt;i&gt;Helicobacter pylori&lt;/i&gt; (&lt;i&gt;H. pylori&lt;/i&gt;) is a common pathogen that has co-evolved with the human host for approximately 100,000 years; however, our understanding of its population structure remains limited. Furthermore, the detailed characteristics of its virulence factors and antibiotic resistance for &lt;i&gt;H. pylori&lt;/i&gt; are not yet fully elucidated.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;In this study, we curated a global genome dataset of 4067 &lt;i&gt;H. pylori&lt;/i&gt; isolates from 76 countries and explored &lt;i&gt;H. pylori&lt;/i&gt; characteristics, including population genetic structure, virulence factors, and antibiotic resistance. We used three approaches (fineSTRUCTURE, ADMIXTURE, and DAPC) to infer the population structure of &lt;i&gt;H. pylori&lt;/i&gt;. We investigated the virulence of each isolate by calling genotypes of &lt;i&gt;cagA&lt;/i&gt; and &lt;i&gt;vacA&lt;/i&gt; and evaluated the correlations of virulence factors with subpopulation. For antibiotic resistance, we identified mutations to determine the genotypic antibiotic resistance. Then we estimated the prevalence of genotypic antibiotic resistance grouped by geographical location, subpopulation, and study period.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Result&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;We identified 21 subpopulations in 4067 &lt;i&gt;H. pylori&lt;/i&gt; isolates, including 20 previously reported subpopulations and a novel subpopulation hspEuropeIsrael, and found that the population structure of &lt;i&gt;H. pylori&lt;/i&gt; was geographically restricted. The novel subpopulation hspEuropeIsrael had a higher proportion of less virulent &lt;i&gt;cagA&lt;/i&gt; and &lt;i&gt;vacA&lt;/i&gt; genotypes compared to other subpopulations. After evaluating the rates of &lt;i&gt;H. pylori&lt;/i&gt; genotypic resistance to four antibiotics, we found that the prevalence of genotypic resistance to amoxicillin and metronidazole was &gt; 15% across all five continents. Genotypic resistance to levofloxacin was &gt; 15% on all continents except for Oceania. Additionally, the genotypic resistance rate to clarithromycin was &gt; 15% in Asia, Europe, and Oceania. A trend of increased genotypic resistance over time was observed in several continents during subgroup analyses. Furthermore, we constructed a comprehensive database for &lt;i&gt;H. pylori&lt;/i&gt;, named &lt;i&gt;Helicobacter Pylori&lt;/i&gt; Encyclopedia for Research (HELPER, http://ccra.njmu.edu.cn/helper).&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Our results provide a detailed characterization of &lt;i&gt;H. pylori&lt;/i&gt; and extend previous schemas. HELPER serves as an informative and comprehensive database that will be a valuable resource for researchers and lay the foundation for future studies on &lt;i&gt;H. pylori&lt;/i&gt;.&lt;/p&gt;\u0000 ","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 2","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143581359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteomic Profiling of Extracellular Vesicles Reveals Potential Biomarkers for Helicobacter pylori Infection and Gastric Cancer","authors":"Phawinee Subsomwong,&nbsp;Krisana Asano,&nbsp;Junko Akada,&nbsp;Takashi Matsumoto,&nbsp;Akio Nakane,&nbsp;Yoshio Yamaoka","doi":"10.1111/hel.70022","DOIUrl":"https://doi.org/10.1111/hel.70022","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p><i>Helicobacter pylori</i> (<i>H. pylori</i>) has been identified as a type I carcinogen and contributes to a high rate of gastric cancer (GC), especially in Eastern Asia. Extracellular vesicles (EVs) have the potential to be used to detect various cancer types and diseases. However, the protein markers in EVs for the prognosis of <i>H. pylori</i> infection and GC are unknown. We aim to identify the proteins within EVs derived from a gastric epithelial cell line (AGS) infected with <i>H. pylori</i> by using LC-MS/MS.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>EVs were isolated from AGS cells infected with high- and low-virulence <i>H. pylori</i> (strains TN2wt and Tx30a) by ultracentrifugation. Proteins within these EVs were identified and analyzed for potential marker candidates through bioinformatics. Proteins in <i>H. pylori-</i>derived EVs (HpEVs) from bacterial culture supernatant and HpEVs derived from <i>H. pylori</i>-infected AGS cells were elucidated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Differentially expressed proteins by proteomic analysis in AGSEVs-Tx30a vs. AGSEVs-noninfected (NI) and AGSEVs-TN2wt vs. AGSEVs-NI were 107 and 55 proteins, respectively. Bioinformatics of these proteomes revealed that essential proteins for <i>H. pylori</i> survival and pathogenicity including outer membrane proteins, metabolism-related, host cell infection-related, and virulence-related proteins were observed in HpEVs. Interestingly, EVs derived from AGS cells infected with <i>H. pylori</i> TN2wt significantly contained multiple proteins related to GC (ATP6V0A1, GAPDH, HINT1, LYZ, and RBX1).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study provides a comprehensive protein profile of EVs from <i>H. pylori</i>-infected AGS cells and HpEVs, which could serve as liquid-based biomarkers in the future for screening <i>H. pylori</i> infection, especially GC-related.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 2","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.70022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143533388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global Prevalence of Helicobacter pylori Infection-Associated Gastric Preneoplastic Lesions in Pediatric Patients: A Systematic Review and Meta-Analysis","authors":"Mohammed Awadh Abdun,&nbsp;Lu Xu,&nbsp;Xiao-Ting Li,&nbsp;Amr Mekky,&nbsp;Maher Al Hussan,&nbsp;Ezaldin M. I. Abuheit,&nbsp;Chen Zhang,&nbsp;Ishtiaq Ur Rahman,&nbsp;Miao Yu,&nbsp;Hafiz Muhammad Sohail Sarwar,&nbsp;Bin-Bin Yan,&nbsp;Jia-Bei Xie,&nbsp;Bo-Wei Liu,&nbsp;Song-Ze Ding","doi":"10.1111/hel.70021","DOIUrl":"https://doi.org/10.1111/hel.70021","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p><i>Helicobacter pylori</i> (<i>H. pylori</i>) is the major cause of gastric mucosal precancerous lesions in adulthood, but its impact on pediatric patients remains unclear. We aimed to investigate <i>H. pylori</i>-induced gastric precancerous lesions in children and adolescents globally and analyze their influencing factors for related disease management and prevention.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>We conducted a comprehensive literature search in major databases to identify studies including pediatric patients with gastric precancerous lesions and <i>H. pylori</i> infection status. Prevalence rates were computed using random-effects or fixed-effect models. A stratified analysis was conducted based on location, age, universal health coverage (UHC), and publication time.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among the 3359 relevant articles screened, 24 studies (7036 participants) met the inclusion criteria. The overall prevalence of precancerous lesions in <i>H. pylori</i>-infected patients was 17.2%, in which atrophic gastritis (AG) and intestinal metaplasia (IM) were 13.5% and 3.6%, respectively. Precancerous lesion rates in infected individuals across different regions were as follows: Africa at 33.8% (AG: 32.6%), Latin America at 22.1% (AG: 17.9%, IM: 4.0%), Asia at 18.1% (AG: 12.4%, IM: 4.4%, Dysplasia: 1.2%), and Europe at 6.3% (AG: 4.3%, IM: 1.7%). Infected adolescents (&gt; 10 years) exhibited a higher prevalence of precancerous lesions than younger children (≤ 10 years) at 14.2% (AG: 9.7%, IM: 2.9%) versus 3.4% (AG: 2.3%, IM: 1.1%), respectively. The prevalence of precancerous lesions in infected patients was higher in areas with low-medium UHC compared with high UHC (24.0% vs. 12.5%).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p><i>H. pylori</i> infection causes significant gastric mucosal precancerous lesions in pediatric patients, representing a major concern for this population and a previously neglected area. Future in-depth investigations and proper management for related disease prevention are warranted.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p> PROSPERO number: CRD42023424683</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143513631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Gastric Microbiota Invade the Lamina Propria in Helicobacter pylori-Associated Gastritis and Precancer","authors":"Harriet J. Giddings,&nbsp;Ana Teodósio,&nbsp;Jordanne Jones,&nbsp;Jack L. McMurray,&nbsp;Kelly Hunter,&nbsp;Riad Alame,&nbsp;Isaac Gardiner,&nbsp;Zainab Abdawn,&nbsp;William Butterworth,&nbsp;Ian R. Henderson,&nbsp;Jeffrey A. Cole,&nbsp;Claire D. Shannon-Lowe,&nbsp;Amanda E. Rossiter-Pearson","doi":"10.1111/hel.70016","DOIUrl":"https://doi.org/10.1111/hel.70016","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Stomach cancer is the fourth leading cause of cancer-related deaths worldwide. <i>Helicobacter pylori</i> is the main risk factor for gastric adenocarcinoma (GAC), yet the precise mechanism underpinning this association remains controversial. Gastric intestinal metaplasia (GIM) represents the precancerous stage and follows <i>H. pylori-</i>associated chronic gastritis (CG). Sequencing studies have revealed fewer <i>H. pylori</i> and more non-<i>H. pylori</i> bacteria in GAC. However, the spatial organization of the gastric microbiota in health and disease is unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>Here, we have combined RNA in situ hybridization and immunohistochemistry to detect <i>H. pylori,</i> non-<i>H. pylori</i> bacteria, and host cell markers (E-cadherin, Mucins 5AC and 2) on tissue sections from patients with CG (<i>n</i> = 15) and GIM (<i>n</i> = 17).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Quantitative analysis of whole slide scans revealed significant correlations of <i>H. pylori</i> and other bacteria in CG and GIM. In contrast to sequencing studies, significantly fewer non-<i>H. pylori</i> bacteria were detected in <i>H. pylori-</i>negative patients. Importantly, whilst <i>H. pylori</i> exclusively colonized the gastric glands, non-<i>H. pylori</i> bacteria invaded the lamina propria in 6/9 CG and 8/10 GIM <i>H. pylori</i>-positive patients. A rapid and cost-effective modified Gram stain was used to confirm these findings and enabled detection of non-<i>H. pylori</i> bacteria in GIM samples.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The invasion of the gastric lamina propria by non-<i>H. pylori</i> bacteria during <i>H. pylori-</i>associated CG and GIM represents an overlooked phenomenon in cancer progression. Further work must determine the mechanisms underlying the synergistic roles of <i>H. pylori</i> and other bacteria in carcinogenesis. This observation should redirect attempts to prevent, diagnose, and treat GAC.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.70016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rebound of Reflux-Related Symptoms After Helicobacter pylori Eradication in Patients With Gastroesophageal Reflux Disease: A Prospective Randomized Study","authors":"Kai-Yu Hu,&nbsp;Ping-Huei Tseng,&nbsp;Jyh-Ming Liou,&nbsp;Chia-Hung Tu,&nbsp;Chien-Chuan Chen,&nbsp;Yi-Chia Lee,&nbsp;Han-Mo Chiu,&nbsp;Ming-Shiang Wu","doi":"10.1111/hel.70023","DOIUrl":"https://doi.org/10.1111/hel.70023","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background/Purpose</h3>\u0000 \u0000 <p>We aimed to assess the effects of <i>Helicobacter pylori</i> (<i>H. pylori</i>) eradication on the rebound of reflux-related symptoms among gastroesophageal reflux disease (GERD) patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This prospective randomized study recruited patients with typical reflux symptoms and reflux esophagitis on esophagogastroduodenoscopy (NCT02934152). Patients positive for <i>H. pylori</i> via a urea breath test (UBT) were randomly assigned to receive bacterial eradication with triple therapy for 2 weeks either before or after proton-pump inhibitor (PPI) treatment for 4 weeks. Follow-up was implemented with serial GerdQ evaluation and a subsequent UBT. The primary outcome was the incidence rates of symptom rebound between patients with and without <i>H. pylori</i> infection. The secondary outcomes included the severity of symptom rebound, incidence rates of symptom rebound, and successful eradication rates between the early and late eradication groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 248 patients were enrolled, of whom 107 (43.1%) tested positive for <i>H. pylori</i> infection. All patients with and without concurrent <i>H. pylori</i> infection had significant symptom improvement over the entire treatment. Patients with <i>H. pylori</i> infection had significantly lower rates of symptom rebound (19.8% vs. 34.2%, <i>p</i> = 0.034) and rebound severity (1.8 ± 0.7 vs. 2.8 ± 1.6, <i>p</i> = 0.031) 4 weeks after eradication and PPI treatment than those without. The incidence rates of symptom rebound and successful eradication rates were not significantly different between the early and late eradication groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>GERD patients with concurrent <i>H. pylori</i> infection were less susceptible to symptom rebound after <i>H. pylori</i> eradication compared to those without.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>ClinicalTrial.gov (NCT02934152)</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}