Helicobacter spp. are gastric or enterohepatic bacteria that can be commensal, opportunistic, or pathogenic. Few studies have evaluated Helicobacter spp. in baboons. Twenty-seven captive baboons were surveyed for Helicobacter spp. by fecal PCR, and a subset evaluated by culture. Nine baboons were treated with oral "triple therapy" with clarithromycin (10 mg/kg), amoxicillin (10 mg/kg), and omeprazole (20 mg) once daily for 10 days. All baboons were positive for Helicobacter spp., including H. macacae (78%), H. suis (19%), and H. pylori (15%). Three novel Helicobacter species were identified by whole genomic sequencing, for which we propose the names Helicobacter papionis, H. simiae, and H. papionifaecis. Treatment was safe and effective for H. pylori, H. suis, and H. macacae, but did not eliminate the novel Helicobacter spp. Species-specific assays should guide treatment of Helicobacter spp. infections in baboons. Further epidemiologic studies are needed to inform clinical management.
The aim of this study was to investigate the effect of PVLWGVPKG (PV9) on gastric mucosa cell damage induced by Helicobacter pylori infection. PV9 intervention could significantly reduce the number of Helicobacter pylori adhering to GES-1 cells (p <0.05). Molecular docking showed that PV9 and its degraded fragments could bind to Helicobacter pylori adhesins, and hydrogen bonds might be the main driving force. Dot blot assays confirmed the binding between PV9 and adhesins SabA and BabA in vitro. The protective mechanism of PV9 against Helicobacter pylori infection-induced GES-1 damage cells was analyzed. It was found that PV9 could accelerate the clearance of reactive oxygen species, reduce mitochondrial membrane potential, improve cell cycle arrest, and prevent apoptosis. In addition, PV9 can also significantly improve the antioxidant capacity of cells (SOD, GSH-Px, and CAT), reducing the content of pro-inflammatory factors (IL-1β, IL-6, IL-8, IL-18, and TNF-α) and increasing the content of anti-inflammatory factors (IL-10). The results of qRT-PCR showed that PV9 could protect GES-1 cells by regulating the expression of apoptotic factors. Moreover, the TLR4/MyD88/NF-κB signaling pathways may play a significant role in this process. This study provides a new idea for antagonizing Helicobacter pylori infection with active peptide components.
Despite increasingly refined diagnostic strategies and regularly updated treatment guidelines, real-world outcomes of Helicobacter pylori management remain variable. Antimicrobial resistance alone does not fully explain these discrepancies, suggesting important challenges in the implementation of evidence-based care. To identify recurring implementation-related challenges across the Helicobacter pylori care pathway and highlight priorities for improving real-world management. This expert-informed review integrated relevant literature, international guideline documents, and structured international expert prioritisation. An initial list of implementation-related pitfalls was developed through literature review, clinical experience, and discussions among the coordinating authors and selected co-authors. Twenty-six experts from five continents participated in a structured consultation process and rated predefined pitfalls using a 5-point Likert scale. Median scores were used for relative prioritisation. Treatment selection and patient management emerged as the domains most consistently prioritised by participating experts. High-impact pitfalls included empirical triple therapy in high-resistance settings, inadequate patient counselling, and empirical retreatment without escalation. Additional challenges were identified across diagnostic, treatment, and follow-up domains, highlighting persistent implementation-related barriers throughout the care pathway. Recurring implementation-related challenges remain important barriers to optimal Helicobacter pylori management. Structured expert prioritisation highlights potential targets for improvement and supports further research and implementation-focused strategies to improve delivery of care.
To investigate the value of combining Helicobacter pylori (HP) virulence factor typing with pepsinogen (PG) in assessing HP infection-related gastric mucosal injury in children. A cross-sectional study enrolled children presenting with gastrointestinal symptoms at Wuxi Children's Hospital from August 2023 to December 2024. Based on gastroscopic pathology, participants were assigned to a mild injury group (n=66) or a moderate/severe injury group (n=51). Serum PG levels and HP virulence factor typing (type I/II) were examined to evaluate the diagnostic performance of combined testing for mucosal injury severity. The moderate/severe injury group had higher serum PGI and PGII levels than the mild injury group (P<0.05), and type I HP infection predominated (85.7%). Receiver operating characteristic curve analysis showed the following diagnostic performance for moderate/severe gastric mucosal injury: type I HP plus PGI positivity yielded an area under the curve (AUC) of 0.781, specificity 62.1%, and sensitivity 82.4%; type I HP plus PGII positivity yielded an AUC of 0.742, specificity 90.9%, and sensitivity 47.1%; simultaneous positivity for type I HP, PGI, and PGII yielded an AUC of 0.775, specificity 60.6%, and sensitivity 82.4%. Serum PG levels and type I HP infection are closely associated with gastric mucosal injury severity. Their combined detection demonstrates good diagnostic performance for grading injury severity and provides a noninvasive strategy for clinical assessment of HP-related gastric mucosal damage in children. 目的: 探究幽门螺杆菌（Helicobacter pylori, HP）毒力因子联合胃蛋白酶原（pepsinogen, PG）对儿童HP感染相关性胃黏膜损伤的评估价值。方法: 采取横断面研究设计，选取2023年8月—2024年12月因消化道症状就诊于无锡市儿童医院的儿童，根据胃镜病理结果分为胃黏膜轻度损伤组（66例）和中/重度损伤组（51例）。检测血清PG水平及HP毒力因子分型（分为Ⅰ/Ⅱ型），分析联合检测对黏膜损伤程度的诊断价值。结果: 中/重度损伤组PGⅠ和PGⅡ水平高于轻度损伤组（P<0.05），且以Ⅰ型HP感染为主（85.7%）。受试者操作特征曲线分析显示，Ⅰ型HP+PGⅠ阳性诊断中/重度胃黏膜损伤的曲线下面积为0.781，特异度为62.1%，灵敏度为82.4%;Ⅰ型HP+PGⅡ阳性诊断中/重度胃黏膜损伤的曲线下面积为0.742，特异度为90.9%，灵敏度为47.1%;Ⅰ型HP+PGⅠ阳性+PGⅡ阳性诊断中/重度胃黏膜损伤的曲线下面积为0.775，特异度为60.6%，灵敏度为82.4%。结论: 血清PG水平和Ⅰ型HP感染与胃黏膜损伤程度密切相关，二者联合检测对胃黏膜损伤程度有较高的诊断效能，为儿童HP感染相关性胃黏膜损伤的临床评估提供非侵入性检查诊断方案。.
Helicobacter pylori is a gram-negative human pathogen that colonizes the stomach and is a major risk factor for gastric ulcers and cancer. A common but poorly understood characteristic of H. pylori is its propensity to aggregate in liquid culture. To investigate this phenomenon, we developed protocols to form, measure, and disperse aggregates. Using these tools, we determined that H. pylori aggregation is protein-dependent and can occur non-clonally, from the binding of distinct cells. Motility, flagella, quorum sensing, and exogenous host proteins were not necessary for aggregation, but the outer membrane proteins AlpA and AlpB were. H. pylori lacking either alpA, alpB, or both were unable to form aggregates. While bacterial aggregation often confers tolerance to antibiotics, H. pylori aggregates were no more tolerant than dispersed cells to several clinically used antibiotics and human serum. Instead, we found that alpA mutants were highly deficient in biofilm formation, suggesting that aggregation may be a step along the H. pylori biofilm formation pathway.IMPORTANCEHelicobacter pylori is a common human pathogen. Infection by this bacterium can lead to gastric cancers and ulcers. H. pylori infections present major global health challenges due to rising antibiotic resistance that complicates treatment. While bacterial aggregation is a recognized driver of antibiotic tolerance and persistence in other pathogens, its role in H. pylori remained unexplored. This work provides the first comprehensive characterization of H. pylori aggregation, demonstrating that it is a protein-mediated but flagella-independent process. We find that, unlike in many other bacteria, aggregation did not confer tolerance to tested antibiotics or serum antimicrobials, but instead may be an initial step on the pathway to forming biofilms. Characterizing H. pylori aggregation is a crucial step toward understanding the microbe's life cycle and may inform novel strategies to disrupt its colonization and persistence.
Helicobacter pylori infection is related to several gastric pathologies, including gastritis, peptic ulcer, and gastric cancer. Substances capable of eradicating H. pylori have been subject to the attention of researchers. This study evaluated a fully characterized ethyl-acetate fraction (EAF), obtained from the rhizomes of L. brasiliense and its microparticulate pharmaceutical form (mpEAF) against H. pylori, and in addition for potential immunomodulatory and antitumor activities associated with H. pylori infection. UHPLC analysis of EAF indicated the presence of samaragenins A and B beside gallic acid, (epi)gallocatechin, epigallocatechin-3-O-gallate. Antioxidant activity showed IC50 values of 5.7 (95% CI: 5.21-6.83), 31.9 (95% CI: 19.57-51.99), and 33.1 (95% CI: 24.4-44.73) µg/mL for HOCl, O2•- and NO, respectively. EAF exerts MIC values of 1024 and 128 µg/mL against the H. pylori (ATCC 43504, clinical isolate P7). In vivo treatments in mice with EAF and mpEAF (100 mg/kg, in single daily doses for 20 consecutive days) improved gastric pathology in infected animals reducing urease positivity (14,3% vs. 54,5% in untreated controls), reducing inflammation (TNF-α, IL-1β, and IL-6 reduced, p < 0.05) and morphological damage compared with the untreated control group. Helicobacter pylori urease was inhibited with IC50 of 521.6 µg/mL (95% CI: 419.2-649.0). In addition, EAF showed antiproliferative activity against gastric adenocarcinoma cells (CC50 of 21.7, 95% CI: 18.1-26.04). In LPS-stimulated macrophages, EAF reduced the TNF-α and IL-6 production by 16% and 35%, respectively. These results indicate the potential of L. brasiliense as a source of compounds capable of attenuating gastric diseases related to H. pylori infection.
The rising global resistance to clarithromycin has substantially reduced the efficacy of empirical Helicobacter pylori eradication regimens. Whether susceptibility-guided tailored therapy offers superior clinical outcomes over empirical therapy remains debated. We systematically searched PubMed, Web of Science, Cochrane Library, Embase, and Scopus from inception to 1 March 2026 for randomized controlled trials comparing susceptibility-guided therapy with empirical therapy for H. pylori infection. The primary outcome was eradication rate; secondary outcomes included any adverse event and specific adverse events. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using a random-effects model. 29 studies were included. Susceptibility-guided therapy significantly improved eradication rates compared with empirical therapy (OR = 1.83, 95% CI: 1.38-2.43; I2 = 74.4%). The benefit was most pronounced in first-line treatment (OR = 2.02, 95% CI: 1.43-2.85), with culture-based phenotypic testing (OR = 2.02, 95% CI: 1.45-2.83), and when compared with triple therapy (OR = 3.41, 95% CI: 2.00-5.80). Ten-day regimens showed the most consistent effect (OR = 1.87, 95% CI: 1.17-3.01; I2 = 29.9%). Susceptibility-guided therapy also reduced the risk of any adverse event (OR = 0.75, 95% CI: 0.57-0.99), particularly abdominal pain, diarrhea, nausea/vomiting, dizziness, abdominal distension, and constipation. Pretreatment antimicrobial susceptibility-guided tailored therapy is more effective than empirical therapy for first-line H. pylori eradication and is associated with fewer adverse events. These findings support integrating susceptibility testing into routine clinical practice.
The changes in the antibiotic resistance patterns of Helicobacter pylori (H. pylori) are critical for guiding clinical eradication therapy. However, data on antibiotic resistance in H. pylori strains isolated from children in Shanghai have been unavailable for the past three years. 676 H. pylori strains isolated from children and relevant clinical information was collected. Antibiotic susceptibility of metronidazole, clarithromycin, levofloxacin and amoxicillin was tested by E-test, resistance gene mutations were detected via PCR and sequencing. Among 676 H. pylori isolates, total resistance rates to metronidazole, clarithromycin, levofloxacin and amoxicillin were 61.5%, 39.1%, 18.2% and 0.3%, respectively. Resistance rates to metronidazole, clarithromycin increased significantly from 2023 to 2025, with increased dual and hetero-resistance. Higher rates of resistance to metronidazole and levofloxacin were observed in the 7-12 year-old group than other two age groups. A2143G in 23S rRNA (98.7%) and N87K in gyrA (61.0%) were the main mutations for clarithromycin and levofloxacin resistance. Over the past three years, a substantial increase in antibiotic resistance toward metronidazole and clarithromycin is observed in H. pylori isolated from children in Shanghai, China.
Early-onset gastric cancer (EOGC), diagnosed before age 45, demonstrates distinct clinicopathological features and poorer prognosis. Current screening strategies lack sensitivity in young populations, while Helicobacter pylori (H. pylori) virulence genotypes (e.g., cagA, vacA) remain underutilized in risk stratification. To develop and validate a diagnostic model combining clinical characteristics and H. pylori virulence serological detection of virulence factors to optimize EOGC risk stratification. In this multicenter case-control study, 200 histologically confirmed EOGC patients and 600 age-matched controls (non-malignant gastric conditions) were enrolled from LiShui Hospital (2023-2024). Clinical parameters, H. pylori infection status (13C-urea breath test), and virulence genotypes (cagA, vacA; ELISA) were analyzed. Multivariable logistic regression identified independent risk factors, followed by risk score development and internal validation (1000 bootstrap replicates). EOGC patients exhibited higher prevalence of persistent epigastric pain (68.5% vs. 32.1%; P<0.001), significant weight loss (6.2 vs. 2.1 kg; P<0.01), and H. pylori infection (85.0% vs. 52.3%; P<0.001). Virulent genotypes were enriched in EOGC: cagA+ (72.5% vs. 45.6%; P<0.01) and vacA s1/m1 (65.0% vs. 38.2%; P<0.01). The final model included five predictors: persistent pain (adjusted odds ratio [aOR]=2.85, 95% CI:1.92-4.23), cagA+ (aOR=3.12, CI: 2.01-4.85), anemia (Hb<110 g/L; aOR=2.34, CI: 1.56-3.51), thrombocytosis (>300×109/L; aOR=1.98, CI: 1.32-2.96), and weight loss >2.1 kg (aOR=2.57, CI: 1.21-2.73). A score ≥3 indicated high risk, achieving 86.5% sensitivity and 82.3% specificity (AUC=0.89, CI: 0.85-0.93). This novel model integrates accessible clinical and microbiological markers to stratify EOGC risk with high accuracy, providing a cost-effective tool for prioritizing endoscopic evaluation in young symptomatic individuals.
Gastric cancer (GC) remains a significant global health burden due to its high incidence and mortality, especially in China. This study aimed to evaluate the performance of combined serological assessment of pepsinogen (PG) and Helicobacter pylori (H. pylori) antibodies for identifying gastric precancerous conditions. From November 2016 to September 2019, an observational cohort study was performed to evaluate serum levels of PG and H. pylori antibodies. Among 19,879 participants, four groups were defined based on serological status: Group A (PG-/ H. pylori-), Group B (PG-/ H. pylori+), Group C (PG+/ H. pylori+), and Group D (PG+/ H. pylori-). Participants from Groups C and D were included in the analysis, while individuals from Groups A and B were randomly selected at a 3:1 ratio relative to Groups D and C, respectively. In total, 1,152 subjects underwent endoscopic and histopathological assessment. Group C demonstrated significantly elevated odds of atrophic gastritis (AG) (OR = 1.98; 95% CI: 1.17-3.26) and intestinal metaplasia (IM) (OR = 1.40; 95% CI: 0.73-2.67) compared to Group A. In the gastric corpus, the odds of AG and IM were 5.0 and 6.8 times higher, respectively, in Group C versus Group A. Combined serological assessment of PG and anti- H. pylori IgG improves the identification of gastric precancerous conditions, with particularly enhanced performance in the gastric corpus.
Amyloidosis is a disease characterized by the abnormal accumulation of amyloids in tissues. The kidneys and heart are the most commonly affected organs in systemic amyloidosis. Primary localized gastric amyloidosis (LGA), on the other hand, is relatively rare. Some past studies have suggested a potential link between Helicobacter pylori infection and LGA, but more research is needed in order to support this hypothesis. A 37-year-old female patient complained of nausea and underwent an endoscopic examination. A 3.0-cm depressed mucosal lesion and mucosal fragility were observed in the upper and posterior gastric wall. She was referred to our hospital with ulcerative bleeding. The silver and Congo red staining results were positive. Echocardiography and abdominal computed tomography were performed to rule out systemic amyloid, and no evidence of systemic involvement was observed. Eradication therapy with standard triple therapy was administered, and successful eradication was confirmed. Two years after the successful eradication, an endoscopic follow-up examination revealed mucosal retraction; however, the mucosal inflammation, including edema and mucosal softening, significantly improved.
Real-time endoscopic diagnosis of Helicobacter pylori infection remains challenging and often requires biopsy-based testing, delaying treatment decisions. Although deep learning (DL) approaches have shown promise, most prior studies have relied on retrospective datasets or image-enhanced modalities, limiting their applicability to routine white-light endoscopy. We aimed to develop and prospectively validate a research-stage DL model for H. pylori detection using only standard white-light endoscopic images. In this single-center prospective study, consecutive adults undergoing diagnostic gastroscopy were enrolled. Six standardized gastric images per patient were targeted under standard white-light endoscopic imaging. Histopathology from antral and corpus biopsies served as the reference standard. An EfficientNet-B0-based DL model was developed to classify H. pylori infection at the patient level by aggregating image-level predictions. Model performance was assessed using five-fold cross-validation within the development cohort, followed by evaluation in an independent temporally separated validation cohort (70% development / 30% temporal validation). A total of 172 patients (1,000 images) were included; 94 patients (54.7%) were H. pylori-positive. In five-fold cross-validation, the model achieved a patient-level AUC of 0.901 (95% CI: 0.863-0.936), with 85.1% sensitivity and 81.4% specificity. In the independent temporal validation cohort (n = 52; prevalence 48.1%), the AUC was 0.889 (95% CI: 0.793-0.960), with 84.0% sensitivity and 85.2% specificity. Aggregating predictions across multiple gastric views improved discrimination compared with single-image inference. In this prospective study, a deep learning model using routine white-light endoscopic images demonstrated reasonable patient-level discrimination for H. pylori detection, including in an independent temporally separated validation cohort. At present, the model should be viewed as a research and decision-support tool rather than a standalone diagnostic system. Multicenter external validation and prospective video-based studies are warranted before routine clinical deployment.
Helicobacter pylori infection affects nearly half of the global population and is a major cause of peptic ulcer disease and gastric cancer. Increasing antibiotic resistance, particularly to clarithromycin, has reduced the efficacy of standard triple therapy, necessitating evaluation of alternative regimens and adjunctive therapies. To compare the eradication rates and safety of clarithromycin- and levofloxacin-based triple therapy, with and without adjunctive lactoferrin. In this randomized, open-label, 2 × 2 factorial trial, 160 adult patients with confirmed H. pylori infection were allocated equally into four groups: clarithromycin-based triple therapy, levofloxacin-based triple therapy, and each regimen combined with lactoferrin. Treatments were administered for 14 days. Eradication was assessed using stool antigen testing four weeks after therapy. Analysis was performed according to the intention-to-treat principle. Eradication rates were 72.5% in both the clarithromycin and levofloxacin groups, compared with 90.0% and 97.5% in the corresponding lactoferrin-supplemented groups, respectively (p = 0.003). Lactoferrin significantly improved eradication rates (72.5% vs. 93.8%, p < 0.001). No significant difference was observed between antibiotic regimens alone (p = 0.673). Adverse events were mild and comparable across groups. Adjunctive lactoferrin significantly enhances H. pylori eradication rates when combined with standard triple therapy, regardless of antibiotic backbone. The evidence proves that lactoferrin should function as an effective adjunct in eradication regimens, particularly in settings of increasing antibiotic resistance.
Helicobacter pylori infection is a major risk factor for gastric cancer (GC), but the molecular mechanisms remain incompletely understood. This exploratory in vitro study investigated whether treatment with the flavonoid morin correlates with altered expression of MAPK/Nrf2/STAT-3 pathway proteins in H. pylori-infected human gastric epithelial cells (GES-1). GES-1 cells were infected with H. pylori (ATCC 49503, MOI 100:1) and treated with 40 µM morin for 24 h. Outcomes included cell viability (MTT assay), ROS production (DCFH-DA), oxidative DNA damage (comet assay), glutathione and malondialdehyde levels (biochemical assays), protein expression (Western blot), and gene expression (RT-PCR). Molecular docking predicted binding affinity between morin and pathway proteins. This study used n = 3 biological replicates per group and a lenient false discovery rate threshold (Q = 0.25) appropriate for hypothesis generation; findings require independent replication. In this exploratory study, morin treatment (40 µM) was associated with: Higher MTT-detectable viability in H. pylori-infected cultures compared to infected untreated controls (85% vs. 45%; q = 0.042) Lower intracellular ROS levels (q = 0.021) and reduced oxidative DNA damage (q = 0.018) compared to infected untreated controls Higher GSH and lower MDA levels compared to infected untreated controls Lower phosphorylation levels of MAPK family members (ERK, JNK, p38), PI3K/AKT, and STAT3/EGFR proteins compared to infected untreated controls Higher total Nrf2 protein expression and upregulation of HMOX1 and NQO1 mRNA compared to infected untreated controls Molecular docking predicted binding between morin and MAPK, STAT3, and NRF2 pathway proteins, but these computational findings require experimental validation. These correlative findings are consistent with the hypothesis that morin treatment engages MAPK/Nrf2/STAT-3 pathways in H. pylori-infected GES-1 cells. However, this study does not establish causality, Nrf2 activation (nuclear translocation not demonstrated), or therapeutic efficacy (no positive controls). The observed associations should be interpreted as hypothesis-generating and require independent replication, mechanistic validation (including Nrf2 loss-of-function experiments), and comparative studies with standard agents before any translational inference. Under the specific in vitro conditions tested (GES-1 cells, H. pylori ATCC 49503, 40 µM morin, 24-h exposure, n = 3 biological replicates), morin treatment was associated with lower ROS levels, reduced MAPK/STAT3 phosphorylation, and higher Nrf2 protein expression compared to infected untreated controls. These correlative findings are hypothesis-generating and do not establish therapeutic potential, safety, efficacy, or clinical relevance. Independent replication, comprehensive toxicological characterization (including normal cell lines and in vivo models), direct comparison with standard agents (clarithromycin, sulforaphane), and mechanistic validation (including Nrf2 loss-of-function experiments) are required before any consideration of morin for further development. This study provides no evidence to support morin as a therapeutic, adjuvant, or alternative agent.
Helicobacter pylori (H. pylori) is a major cause of gastric cancer (GC); however, GC also develops in H. pylori-negative patients, and the characteristics of non-H. pylori microbial communities remain unclear. We characterized gastric microbiota in patients with GC according to H. pylori status, sex, GC subtype, and longitudinal changes following H. pylori eradication therapy. Gastric corpus mucosal samples were collected from 35 patients with GC who underwent endoscopic therapy and longitudinal follow-up. Some patients were followed for more than 10 years, and gastric microbiota were analyzed using 16S rRNA gene sequencing. H. pylori-negative samples exhibited significantly higher microbial diversity and distinct community structures compared with H. pylori-positive samples, which was consistent across sex and GC subtypes. Multiple non-H. pylori taxa were enriched in H. pylori-negative samples, including organisms with reported urease and nitrate-reducing activities. Longitudinal analyses demonstrated that successful eradication induced significant but non-uniform microbial shifts, whereas persistent infection maintained stable H. pylori-dominated profiles. Notably, species-level analyses revealed selective and H. pylori eradication-specific microbial changes, with Actinomyces naeslundii consistently enriched only in the H. pylori eradicated group across longitudinal modeling and differential abundance analyses. Functional prediction analyses revealed a reduced representation of host-pathogen interaction-related pathways in H. pylori-negative samples. These findings suggest that H. pylori-negative gastric microbiota harbor functionally distinct microbial communities that may contribute to gastric carcinogenesis through alternative microbial and ecological pathways. In addition, H. pylori eradication revealed a longitudinal remodeling of gastric microbiota.
Taiwan has launched community-based Helicobacter pylori (H. pylori) screening programs in select areas. However, in many parts of Taiwan, the most effective treatment strategies remain unclear. In July 2023, H. pylori stool antigen (HpSA) screening for adults aged 50-69 years was added to the county-wide community-based health promotion program conducted by the Chiayi County Health Bureau. This single-center retrospective analysis included 531 HpSA-positive individuals who were evaluated at Chiayi Chang Gung Memorial Hospital between July 2023 and June 2024. Among the 5749 screened adults aged 50-69 years in Chiayi County, HpSA positivity was 25.6% (95% CI, 24.5-26.7). Of 1470 HpSA-positive individuals identified through screening, 531 (36.1%) were evaluated at the study hospital. Of them, 458 (86.3%) underwent endoscopy, which identified gastric ulcers in 24.5%, duodenal ulcers in 17.0%, and both in 6.6%. Rapid urease test and histological assessment were performed in 316 and 158 patients, respectively, yielding a positivity rate of 87.0% and 86.7% respectively. Among the 441 patients with available follow-up data, eradication rates were 94.7% (216/228) for those receiving 14-day clarithromycin-based triple therapy and 93.1% (149/160) for those receiving pooled 7-14-day concomitant therapy (p = 0.508). Reverse hybrid therapy achieved a 100% eradication rate in 20 patients, without significant difference compared to triple therapy (p = 0.293). Among screened adults aged 50-69 years in Chiayi County, HpSA positivity was approximately 25.6%. Fourteen-day triple therapy, 7-14-day concomitant therapy and reverse hybrid therapy all achieved high eradication rates.
We delineated the relationship between body mass index (BMI) and incidences of Helicobacter pylori infection in overweight (obese) and normal weight asymptomatic individuals. This cross-sectional study involved participants who had undergone health checkups for H. pylori infections between January 2013 and December 2017. The association between gender, age, BMI and H. pylori infection prevalence was investigated. In total, 41,454 subjects were enrolled in this study. The overall H. pylori infection prevalence was 42.5%, 48.0%, 50.7% and 54.9% in under weight, normal weight, pre-obese, and obese individuals, respectively. Pre-obesity/obesity (OR = 1.15; 95%CI 1.10 to 1.20; P < .001) was correlated with increased H. pylori infection prevalence compared to subjects with normal weight. Increased BMI (OR = 1.04; 95%CI 1.03 to 1.06; P < .001) was also correlated with increased H. pylori infection prevalence compared to individuals with normal weight. However, Subgroup analysis indicated that there are no relationship between BMI and H. pylori infection prevalence in individuals with age < 30 among all subjects (OR = 1.01; 95%CI 0.99 to 1.03; P = .282). Increased BMI is correlated with increased H. pylori infection prevalence among individuals with age of 30 or more years.
Neurological disorders are increasingly linked to dysfunction of key cellular organelles, including mitochondria, endoplasmic reticulum (ER), lysosomes, endosomes, and peroxisomes. These organelles coordinate essential neuronal processes via tightly regulated crosstalk. Disruption in one organelle can propagate dysfunction across others, amplifying neurodegenerative cascades. Emerging evidence suggests that neurological diseases can result not only from disturbances in brain homeostasis but also from imbalances in gut homeostasis, highlighting the significant role of the gut-brain axis in maintaining neurological health. Helicobacter pylori, a gut pathogen contribute to the progression of neurological modalities by its secretome comprising Vac A, CagA, urease, and outer membrane vesicles via perturbing organelle function. These virulence factors induce mitochondrial fragmentation, ER stress, lysosomal dysfunction, and impaired mitophagy, disrupting organelle networks and promoting synaptic loss and neuronal death. Understanding how pathogen-induced organelle stress contributes to neurodegeneration offers novel insights into infection-driven brain disorders.
Helicobacter pylori is a common chronic bacterial infection primarily associated with gastrointestinal disease. Increasing evidence suggests that H. pylori may also exert systemic effects beyond the stomach, including possible modulation of neuroendocrine pathways. This study aimed to investigate the association between H. pylori infection and alterations in serum cortisol and thyroid-stimulating hormone (TSH) levels as indicators of hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-thyroid (HPT) axis activity. In this case-control study, 850 adults were enrolled, including 425 H. pylori-positive cases and 425 H. pylori-negative controls. Active H. pylori infection was determined using a monoclonal stool antigen test (HpSA). Fasting venous blood samples were collected between 08:00 and 10:00 AM under standardized conditions. Serum cortisol and TSH levels were measured using validated immunoassays. Group comparisons, correlation analysis, sex-stratified subgroup analysis, and receiver operating characteristic (ROC) curve analysis were performed. H. pylori-positive participants had significantly higher serum cortisol levels and lower TSH levels compared with controls (both p < 0.001). A significant inverse correlation between cortisol and TSH was observed only in infected participants (r = -0.41, p < 0.001). These hormonal alterations were evident in both sexes. ROC analysis showed moderate discriminatory performance for cortisol (AUC = 0.71) and fair-to-moderate performance for TSH (AUC = 0.67). H. pylori infection was significantly associated with elevated cortisol levels, reduced TSH levels, and an inverse relationship between both hormones in adults. These findings suggest that chronic H. pylori infection may influence both HPA and HPT axis regulation and support further investigation into its systemic neuroendocrine effects.
Helicobacter pylori (H. pylori) is a globally prevalent gastric pathogen whose increasing antimicrobial resistance has reduced the efficacy of conventional eradication regimens. Bacteriophages and phage-derived products have therefore attracted growing interest as alternative antimicrobial strategies against H. pylori. However, progress in this field remains constrained by the limited availability of cultivated phages, the underexplored reservoir of prophages and uncultivated phages, narrow host range, and poor stability under gastric conditions. In this review, we summarize the current landscape of H. pylori phage research, including both virulent and temperate phages, and discuss how genome-based mining is expanding access to previously inaccessible phage resources. We further examine recent application-oriented advances, including artificial intelligence-assisted endolysin discovery, receptor-binding protein engineering for host-range expansion, and targeted delivery platforms designed to improve phage stability and site-specific activity in the stomach. Finally, we highlight key translational barriers, including biosafety evaluation, functional validation, and in vivo efficacy. Together, these advances provide a framework for evaluating phage-based and phage-derived antimicrobial strategies for H. pylori control, while highlighting the need for rigorous functional validation, biosafety assessment, and in vivo efficacy testing.