Search Results (1,034)

Background: Liver cirrhosis is associated with portal hypertension and its gastrointestinal complications, but non-variceal gastroduodenal mucosal injury and its relationship to Helicobacter pylori (H. pylori) infection and hepatic disease severity remain incompletely characterized. Methods: This retrospective, cross-sectional study included 162 patients undergoing first upper gastrointestinal endoscopy (61 with cirrhosis, 101 controls), assessed using a composite gastroduodenal mucosal injury score (range 0–16) across the antrum, gastric corpus, duodenal bulb, and second duodenal portion. Results: Cirrhosis was independently associated with a higher injury burden after adjusting for H. pylori status, nonsteroidal anti-inflammatory drug (NSAID), antiplatelet, anticoagulant, and proton pump inhibitor (PPI) use (adjusted count ratio [aCR] = 1.33, 95% CI: 1.09–1.63, p = 0.006); and H. pylori infection was independently and separately associated with higher injury burden (aCR = 1.25, 95% CI: 1.01–1.54, p = 0.037), while none of the four medication classes showed an independent association. This excess injury was concentrated almost exclusively in the gastric corpus (adjusted aCR = 3.04, p < 0.0001), with no significant differences at other sites. Injury severity did not correlate with Child–Pugh class or tests of the liver’s biosynthetic capacity (all p > 0.05). Only patients with concurrent cirrhosis and H. pylori infection showed significantly elevated injury relative to unexposed controls (adjusted aCR = 1.87, 95% CI: 1.38–2.53, p < 0.0001), with a significant, exploratory cirrhosis × H. pylori interaction (aCR = 1.56, p = 0.037). Conclusions: Cirrhosis is therefore associated with a corpus-predominant pattern of gastroduodenal injury, compatible with, though not proof of, a portal hypertension-related mechanism, and shows a significant positive multiplicative interaction with concurrent H. pylori infection; given the exploratory nature of this analysis, these findings are hypothesis-generating and warrant prospective confirmation before informing endoscopic screening or infection-screening practice. Full article

Background: Helicobacter pylori infection is a common chronic bacterial infection and an established cause of gastritis, peptic ulcer disease, and gastric cancer. Environmental and host metal status may interact with gastric inflammatory and microbial processes, and infection-related changes in gastric acidity, mucosal permeability, and metal handling may in turn alter local tissue concentrations. This study compared systemic and gastric tissue concentrations of seven elements in adults with histopathologically confirmed H. pylori infection and uninfected controls. Methods: This single-center case–control study included 110 adults undergoing upper gastrointestinal endoscopy (55 H. pylori-positive and 55 H. pylori-negative). H. pylori status was established by hematoxylin–eosin and modified Giemsa staining. Whole blood collected in purple-top K₂EDTA tubes was analyzed for As, Pb, Cd, and Sn; serum obtained from yellow-top serum-separator tubes containing clot activator and separator gel was analyzed for Al, Co, and Ni. A separate fresh antral biopsy, not the formalin-fixed histology specimen, was used for ICP-MS; tissue concentrations were normalized to recorded dry weight. Between-group metal comparisons were corrected as one family of 14 tests using Benjamini–Hochberg FDR. Prespecified age- and sex-adjusted models and an exploratory multivariable model were supplemented by ROC, PCA, and internally cross-validated PLS-DA analyses. Results: The H. pylori-positive group was older than the negative group (55.65 ± 15.01 vs. 52.42 ± 12.53 years). Blood aluminum was nominally higher in the positive group (p = 0.032; q = 0.112). In gastric tissue, aluminum was higher [0.23 (0.13–13.40) vs. 0.13 (0.10–0.23) μg/g dry weight; p < 0.001; q = 0.002], whereas arsenic was lower [1.35 (0.54–2.02) vs. 1.92 (1.47–2.43) μg/g dry weight; p < 0.001; q = 0.003] in H. pylori-positive participants. Tissue cobalt and blood/tissue nickel differences did not remain significant after FDR correction. In prespecified age- and sex-adjusted models, tissue arsenic showed an inverse association (OR = 0.431, 95% CI 0.263–0.705; p = 0.0008), whereas tissue aluminum showed a positive association (OR = 4.957, 95% CI 1.629–15.085; p = 0.0048). In the exploratory joint model, only tissue aluminum remained significant (adjusted OR = 4.016, 95% CI 1.119–14.417; p = 0.033). The joint model had an apparent within-cohort AUC of 0.774; repeated five-fold cross-validated PLS-DA yielded an AUC of 0.707. Conclusions: Histopathologically confirmed H. pylori status was associated with compartment-specific metal concentration patterns, particularly higher tissue aluminum and lower tissue arsenic. Because the study was cross-sectional and measured total concentrations, these findings do not establish environmental exposure, temporal accumulation, toxicity, or a causal direction. The regression and multivariate findings are exploratory and require validation in independent cohorts with standardized tissue sampling, arsenic speciation, exposure assessment, and quantitative gastric pathology. Full article

Background and Objectives: Ménétrier’s disease (MD) is an exceptionally rare hypertrophic gastropathy characterized by foveolar hyperplasia, gastric acid suppression, and protein-losing enteropathy. Congenital gallbladder duplication is a rare biliary anomaly associated with independent pathological risks and surgical complications. Case Presentation: We report the case of a 34-year-old male presenting with chronic epigastric and right hypochondriac pain, alongside persistent, uninvestigated polycythemia. Upper endoscopy and histopathology revealed diffuse foveolar hyperplasia with cystic oxyntic gland dilatation and active Helicobacter pylori infection, confirming MD. Magnetic resonance cholangiopancreatography demonstrated a double gallbladder with independent cystic ducts. Successful H. pylori eradication was achieved, and hematological workup ruled out primary myeloproliferative neoplasm. Conclusions: To our knowledge, this is the first reported case of concurrent MD, and double gallbladder. This report underscores the necessity of a systematic diagnostic approach combining advanced imaging and histopathology to manage complex, overlapping abdominal pathologies. Full article

Chronic infection with Helicobacter pylori (H. pylori) is a major environmental risk factor for gastric carcinogenesis. Malignancy is largely driven by variations within the virulence factor CagA, with East Asian lineages exhibiting higher oncogenic potential than Western ones. However, how these variants modulate cellular crosstalk remains poorly understood. We integrated molecular dynamics (MD) simulations with single-cell transcriptomics across progressive disease stages, including chronic atrophic gastritis, intestinal metaplasia, and gastric cancer. Local niche remodeling was evaluated via cell–cell communication profiling among epithelial, stromal, and immune circuits, while simulations of MARK2 kinase bound to distinct CagA lineages determined binding affinities. Single-cell analysis revealed that H. pylori toxicity progressively dampens epithelial–stromal crosstalk, marked by severe epithelial polarity aberrations that disrupt neuroendocrine-like secretory and synaptic pathways during malignant transformation. Mechanistically, MD simulations and MM/GBSA calculations demonstrated that East Asian CagA lineages exhibit higher binding affinity toward host MARK2 than Western lineages. Specific East Asian amino acid substitutions dramatically tighten the protein interface, driving stronger signaling perturbations. This study bridges atomistic structural virulence with microenvironmental shifting, establishing geographic CagA toxicity divergence as a critical determinant for pathogen-driven gastric cancer risk. Full article

Helicobacter pylori infection is a major cause of gastric cancer, and eradication before advanced precancerous gastric changes develop provides a biologically plausible opportunity for primary prevention. Adolescence represents a strategically favorable, although not universally established, window for intervention in Japan because persistent childhood-acquired infection can be identified before extensive mucosal damage while school-based programs provide organized access to defined birth cohorts. This narrative review evaluates the evidence supporting population-based adolescent H. pylori screening, its potential harms and uncertainties, and the lessons derived from Japanese implementation. Representative programs demonstrate that organized screening is feasible but show substantial heterogeneity in participation, diagnostic pathways, antimicrobial resistance, eradication outcomes, and retention across the care cascade. Direct evidence that adolescent screening reduces future gastric cancer incidence or mortality is not yet available. As H. pylori prevalence declines, the balance among screening yield, diagnostic performance, antimicrobial exposure, cost, and equity will continue to change. International experience further indicates that prevention strategies should be matched to local epidemiology and healthcare systems. Adolescent screening should therefore be viewed as an adaptive prevention strategy whose target population, diagnostic pathway, and treatment approach require periodic reassessment. Full article

Functional fermented foods are increasingly recognized as sources of microbial metabolites with potential biological activity. In this study, MRK2-3, a protease-sensitive anti-Helicobacter pylori component produced by Lactiplantibacillus pentosus MRK2-3 isolated from fermented mushroom sausage, was enriched and preliminarily characterized for in vitro anti-H. pylori activity. Activity appeared during the stationary phase. Sequential ethyl acetate extraction, Sep-Pak C18 chromatography, and reverse-phase HPLC increased specific activity, although the final activity recovery was 0.72%. MALDI-TOF analysis of the active fraction showed a dominant ion at approximately m/z 1848 together with several lower-intensity ions; therefore, chemical homogeneity and sequence identity were not established. The MRK2-3 fraction retained activity after incubation at pH 2–6 and after heating at 80 °C and 100 °C for 30 min, whereas activity decreased under alkaline conditions and after treatment at 121 °C for 15 min. Trypsin, α-chymotrypsin, pepsin and proteinase K reduced activity. The fraction inhibited all tested H. pylori strains (agar-dilution MIC ranged from 12.5 to 100 μg/mL). In a simulated gastric fluid, higher concentrations produced a rapid reduction in viable H. pylori 3949 counts. These findings support MRK2-3 as a fermentation-derived putative antimicrobial peptide candidate with anti-H. pylori activity under gastric-like conditions. However, its amino acid sequence, structural identity, and novelty require confirmation. Antimicrobial mechanism, cytotoxicity, and in vivo efficacy also remain to be established. Full article

Background: Synbiotics may improve the effectiveness of antibiotic-based Helicobacter pylori eradication therapy; however, the available evidence remains limited. This systematic review and meta-analysis updated the evidence on the efficacy and safety of adjunctive synbiotics for H. pylori eradication and treatment-related adverse events. Methods: This systematic review and meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA 2020) guidelines and was registered in PROSPERO (CRD420251236314). PubMed, Scopus, Embase, MEDLINE, Web of Science, and Google Scholar were searched from inception to their respective final search dates in November and December 2025 for randomized controlled trials comparing antibiotic-based eradication therapy plus a synbiotic with the corresponding regimen without synbiotics. Risk ratios (RRs) with 95% confidence intervals (CIs) were pooled for intention-to-treat (ITT), per-protocol (PP), and safety outcomes. Risk of bias was assessed using the Cochrane Risk of Bias 2 tool, and certainty of evidence was evaluated using the GRADE approach. Results: Six randomized controlled trials enrolling 486 participants were included; 446 participants contributed to the ITT analysis and 416 to the PP analysis. One trial was judged to be at high risk of bias, whereas five raised some concerns. The ITT analysis demonstrated improved eradication with adjunctive synbiotics (RR 1.18, 95% CI 1.04–1.34; I² = 44.53%). No significant benefit was observed in the PP analysis (RR 1.06, 95% CI 0.95–1.18; I² = 48.40%). Safety data were available from three pediatric trials (n = 230), with low-certainty evidence suggesting fewer overall adverse events (RR 0.27, 95% CI 0.16–0.45). Conclusions: Adjunctive synbiotics may modestly improve H. pylori eradication and may reduce overall adverse events. However, the eradication benefit was not confirmed in PP analyses, and the safety findings should be interpreted cautiously given the limited pediatric evidence. Full article

Gastric cancer is one of the malignancies with the highest incidence and mortality worldwide. Helicobacter pylori (H. pylori) infection is the primary driving factor in its development. The progression of gastric mucosal malignancy follows the Correa cascade model: “chronic non-atrophic gastritis → chronic atrophic gastritis (CAG) → intestinal metaplasia (IM) → dysplasia (Dys) → gastric cancer.” Currently, clinical management faces major challenges, including increasing antibiotic resistance in H. pylori, limited pharmacological options for gastric precancerous lesions, and treatment resistance and toxicity in established gastric cancer. This review synthesizes current evidence on BBR, COP, EPI, PAL, and JAT and organizes their reported actions into a three-tier intervention framework. At the first tier, etiologic and inflammatory interception, individual alkaloids suppress H. pylori persistence through direct antibacterial injury, urease inhibition, and modulation of bacterial virulence and antibiotic susceptibility, while attenuating infection-driven inflammatory and immune responses. At the second tier, modulation of precancerous mucosal progression, preclinical studies indicate that these compounds can ameliorate gastric glandular injury and may attenuate biological processes associated with progression toward intestinal metaplasia and dysplasia. At the third tier, antitumor and adjunctive intervention in established gastric cancer, alkaloids inhibit proliferation, induce cell-cycle arrest and apoptosis, suppress invasion and metastasis, and regulate non-coding RNA and epigenetic networks; BBR-centered preclinical studies further suggest potential chemosensitizing and supportive effects. This review integrates the five alkaloids BBR, COP, EPI, PAL, and JAT and systematically elucidates their mechanisms of action across the pathological continuum from H. pylori infection and chronic inflammation to precancerous lesions and ultimately gastric cancer. It establishes a stage-oriented, compound-specific analytical framework to clarify the pharmacological positioning of these compounds, identify priorities requiring further validation, and guide future mechanistic and translational research. Full article

Helicobacter pylori is one of the most common bacterial pathogens in humans and the primary etiological agent of chronic gastritis, peptic ulcer disease, and gastric cancer. Its ability to establish persistent gastric colonization relies on multiple virulence factors, including adhesins, urease, cytotoxins, motility, outer membrane vesicles, and biofilm formation, which collectively promote bacterial survival, chronic inflammation, and treatment failure. The increasing prevalence of antibiotic-resistant H. pylori strains has intensified the search for therapeutic strategies targeting both bacterial viability and virulence. Berberine (BBR), a natural isoquinoline alkaloid, has emerged as a promising candidate because of its antibacterial, anti-inflammatory, and antioxidant properties. Increasing evidence derived from native berberine, its derivatives, and berberine-based formulations indicates multifaceted anti-H. pylori activity, including direct antibacterial effects, inhibition of virulence determinants, and modulation of host inflammatory responses. This review summarizes current knowledge on the epidemiology and pathogenic mechanisms of H. pylori and provides a comprehensive overview of the available evidence regarding the anti-H. pylori pharmacological profile of BBR-based compounds. Particular attention is given to their effects on bacterial adhesion, motility, urease activity, efflux pump function, biofilm formation, and host inflammatory signaling pathways. The review also discusses findings from preclinical and clinical studies supporting BBR-based strategies as adjuncts to conventional eradication therapies. In addition, recent advances in nanotechnology-based drug delivery systems designed to overcome the poor oral bioavailability of BBR and improve its therapeutic efficacy against H. pylori are highlighted. Full article

Background/Objectives: Delonix regia seeds contain phytochemicals with therapeutic potential, but their activity against Helicobacter pylori and biomedical properties remain incompletely characterized. This study aimed to characterize the phenolic and amino acid composition of D. regia seed extract (DRSE) and evaluate its anticancer, wound-healing, anti-inflammatory, anticoagulant, antibacterial, antibiofilm and urease-targeted docking activities. Methods: DRSE was analyzed by high-performance liquid chromatography (HPLC) and amino acid analysis. Biological effects were assessed using MTT cytotoxicity, scratch wound-healing, bovine serum albumin (BSA) denaturation, prothrombin time (PT) and partial thromboplastin time (PTT), antibacterial and crystal violet antibiofilm assays. Gallic acid and vanillin were docked against H. pylori urease (PDB ID: 1E9Y). Results: Gallic acid was the predominant phenolic compound (1417.90 µg/g), while aspartic and glutamic acids dominated the amino acid fraction. DRSE showed preferential cytotoxicity toward A431 carcinoma cells (IC₅₀ = 108.97 ± 0.68 µg/mL) compared with HFB4 fibroblasts (IC₅₀ = 318.56 ± 2.06 µg/mL), yielding a selectivity index of 2.92. Scratch closure was comparable to the control (81.71% versus 80.85%), although the migration rate increased to 16.12 µm. DRSE inhibited protein denaturation by 91.20% (IC₅₀ = 6.39 ± 0.19 µg/mL) and prolonged PT and PTT to 27.37 and 90.50 s, respectively. It inhibited H. pylori with minimum inhibitory and bactericidal concentrations of 31.25 µg/mL and suppressed biofilm formation by 95.39%. Gallic acid and vanillin showed comparable urease docking scores of −4.72 and −4.71 kcal/mol. Conclusions: DRSE showed selective anticancer, anti-H. pylori, antibiofilm, anti-inflammatory, anticoagulant, and moderate pro-migratory activities. Mechanistic, safety and in vivo studies are warranted. Full article

Helicobacter pylori (H. pylori) eradication with bismuth-containing quadruple therapy (BQT) is effective but often accompanied by adverse gastrointestinal reactions and gut microbiota disturbances, while the impact of probiotic supplementation and the predictive value of the gut microbiota remain incompletely understood. In this single-center prospective randomized controlled trial, 109 H. pylori-positive patients were assigned to receive a 14-day BQT alone treatment or BQT combined with compound Lactobacillus acidophilus (LBQT). Fecal samples were collected before treatment, at the end of therapy, and four weeks after completion for 16S rDNA amplicon sequencing to assess microbiota dynamics. Although the addition of compound L. acidophilus did not significantly alter eradication rates, it markedly reduced the incidence of gastrointestinal adverse reactions, accelerated the recovery of gut microbial diversity and abundance, and delayed the overgrowth of potentially pathogenic bacteria, as well as increased short-chain fatty acid-producing bacteria. We further predicted the success of H. pylori eradication using ROC curves, and found that the combined baseline fecal microbiota markers (o_Lactobacillales, o_Enterobacterales, and f_Enterobacteriaceae) achieved an AUC of 0.849 at the start of treatment; at 4 weeks after eradication, the AUC of the microbiota combined with o_Peptostreptococcales, c_Bacilli, o_Lactobacillales, and g_Streptococcus predicted successful eradication up to 0.776. These findings indicate that compound L. acidophilus supplementation alleviates the side effects of BQT and promotes the restoration of gut microbiota homeostasis, and that gut microbiota signatures may serve as noninvasive predictors of treatment tolerance and therapeutic outcome. Full article

Gastric mucosa-associated lymphoid tissue (MALT) lymphoma, also known clinically as gastric MALT lymphoma (GML) or MALToma, is an indolent B-cell neoplasm strongly associated with chronic Helicobacter pylori (H. pylori) infection. While early-stage disease is based on persistent antigenic stimulation and chronic inflammation, the metabolic and molecular transitions that drive monoclonal B-cell autonomy remain poorly understood. Importantly, H. pylori maintain this long-term colonization by defusing the host’s innate immunity; specifically, its lipid A portion features unique elongated acyl chains, composed of 16–18 carbon atoms, that fail to bind to and activate host TLR4/MD2 receptors, resulting in exceptionally weak endotoxic potency. Persistent colonization relies on key oncoproteins, particularly cytotoxin-associated gene A (CagA) and vacuolar cytotoxin A (VacA), which orchestrate early inflammatory infiltration (neutrophils, Th1, Th2 and Th17 cells) before shifting the microenvironment toward a suppressive regulatory T cell (Treg) phenotype. In this study, we propose a new critical step in the oncogenesis of gastric metastasis: chronic mitochondrial and immunometabolic adaptation within the gastric microenvironment. We claim that H. pylori act not only as a trigger for infection but also as a chronic driver of mitochondrial adaptation to oxidative stress and hypoxia, which subsequently results in defective mitophagy. CagA- and VacA-mediated mitochondrial damage induces reactive oxygen species (ROS) and functional hypoxia, stabilizing HIF-1α to force a glycolytic metabolic shift, while incomplete mitophagy rescues metabolically altered, apoptosis-resistant clones to drive monoclonal B-cell expansion. Within this ecological-microenvironmental framework, the predominantly cytoplasmic sequestration of BCL10 and the NF-κB subunit p65 observed in GML is reinterpreted not as evidence of signaling inactivity, but as a dynamically regulated adaptive state. This configuration is orchestrated by mitochondrial stress responses that enable adaptation to the chronic microenvironmental pressures imposed by H. pylori, acting in concert with the metabolic programs governed by MYC, NRF2, and BCL2. Overall, this review outlines the multi-step pathogenesis of H. pylori-mediated GML, highlighting how mitochondrial dysfunction and metabolic remodeling drive the transition from chronic infection to malignant transformation. Full article

Background: Antibiotic resistance in Helicobacter pylori is steadily increasing, rendering the treatment of related gastroduodenal diseases increasingly difficult. Lefamulin is a new broad-spectrum antibacterial in the pleuromutilin class, acting by suppressing bacterial protein synthesis. It has the advantages of its unique “induced-fit” mechanism, a low frequency of spontaneous mutations, stepwise development of resistance, stability in acidic environments, and potential for additive or synergistic activity when combined with certain other antibiotics against various facultative anaerobes, including multidrug-resistant isolates. Methods: We investigated, for the first time to the best of our knowledge, the activity of lefamulin against 91 clinical H. pylori isolates from symptomatic adult patients using MIC test strips. Results: Overall, lefamulin MICs₅₀ and MICs₉₀ were 0.25 and 2 mg/L versus 4 and ≥256 mg/L for clarithromycin, and 0.75 and ≥32 mg/L, respectively, for levofloxacin. Lefamulin MICs₅₀ and MICs₉₀ were 0.5 mg/L and 4 mg/L against the 61 clarithromycin-resistant (MICs, >0.25 mg/L) isolates, 0.25 and 0.75 mg/L against the 40 levofloxacin-resistant (MICs, >1 mg/L) isolates, and 0.38 mg/L and 0.75 mg/L, respectively, against the 28 isolates resistant to both agents. Conclusions: Briefly, the new pleuromutilin antibiotic outperformed in vitro both clarithromycin and levofloxacin against H. pylori isolates. Its potential usefulness in treating H. pylori infections resistant to macrolides and fluoroquinolones, and especially those with dual resistance, justifies further investigation. However, some precautions should also be considered. The use of the novel antibiotic lefamulin may offer benefits for H. pylori eradication if our results are confirmed in subsequent studies, including clinical trials. Full article

Helicobacter pylori is a cholesterol-auxotrophic pathogen capable of internalizing into Candida albicans, where the yeast may serve as a protective intracellular niche under adverse environmental conditions. Because ergosterol is an analog of cholesterol, this study investigated its contribution to the interaction between H. pylori J99 and C. albicans ATCC 90028. Ergosterol was extracted from the wild-type strain ATCC 90028 and from Δerg4, Δerg5, and Δerg6 mutants, identified and quantified by UHPLC-MS/MS, and evaluated for its effects on bacterial viability, growth, chemotaxis, and intracellular internalization. Ergosterol showed no inhibitory effect on H. pylori viability within the tested concentration range. Ergosterol extracted from C. albicans ATCC 90028 enhanced bacterial growth and induced a rapid positive chemotactic response comparable to that elicited by cholesterol, whereas ergosterol-deficient mutants produced weaker responses. Internalization assays demonstrated that reduced ergosterol availability significantly decreased bacterial entry into yeast cells. These findings identify ergosterol as a key determinant of the H. pylori–C. albicans interaction, supporting the hypothesis that fungal sterols facilitate bacterial chemotaxis and intracellular persistence. This work provides new insights into the molecular basis of bacterial–fungal endosymbiosis and suggests that ergosterol-mediated interactions may contribute to the persistence and transmission of H. pylori. Full article

Background: Among natural products, vanillin (Van), a major component of Vanilla planifolia, exhibits multiple bioactivities, including antimicrobial effects. Methods: In this study, Van, its analogues o-vanillin (oVan), iso-vanillin (iVan), ethylvanillin (eVan), and a library of newly synthesized derivatives were evaluated against Helicobacter pylori strains with distinct antibiotic susceptibilities. Time-kill kinetics, antibacterial spectrum, and viability in a normal gastric cell line GES-1, were also assessed. Results: Van showed minimal or no activity (MIC and MBC > 128 µg/mL), whereas structural modifications markedly improved anti-H. pylori activity, with MIC values as low as 4 µg/mL. Compounds 16V, 20oV, and 29eV were among the most potent (MIC₉₀ = 4–16 µg/mL). Activity depended on both the vanilloid core and substituent type. The compounds were inactive against representative Gram-negative and Gram-positive bacteria (MIC > 128 µg/mL). Selected compounds preserved viability in GES-1 cells. Hierarchical clustering, artificial neural clustering, and principal component analysis identified potency-related architectural motifs and strain-specific activity. Docking against H. pylori urease suggested that several compounds, particularly 16V, may interact with the enzyme, providing preliminary support for a possible involvement of this target. Conclusions: Systematic modification of the vanilloid scaffold generated selective and relatively non-cytotoxic anti-H. pylori hit compounds and confirmed the value of natural metabolites in antibacterial drug discovery. Full article