Frontiers in Microbiology
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2022
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IF 6.064
Jia Xiaofen,Huang Qiuyue,Lin Miaomiao,Chu Yingming,Shi Zongming,Zhang Xuezhi,Ye Hui
Background: Helicobacter pylori (H. pylori) infects half of the human population globally. Eradication rates with triple or quadruple therapy have decreased owing to the increasing rate of antibiotic resistance. Jinghua Weikang capsule (JWC) is the first and most popular Chinese patent medicine approved by the state for the treatment of gastritis and peptic ulcers caused by H. pylori infection in China. Previous studies have found that JWC has a certain bactericidal effect on drug-resistant H. pylori and its major component, Chenopodium ambrosioides L. inhibits biofilm formation, but the mechanism remains unclear. This study focused on drug-resistant H. pylori and explored whether JWC could reverse drug resistance and its related mechanisms.Method: The agar plate dilution method, E-test method, and killing kinetics assay were used to evaluate the bactericidal effect of JWC on antibiotic-resistant H. pylori and its effect on antibiotic resistance. Sanger sequencing was used to detect mutations in drug resistance genes. The crystal violet method, scanning electron microscopy, and confocal laser scanning microscopy were used to evaluate the effects of JWC on biofilms. qPCR was performed to evaluate the effect of JWC on the expression of efflux pump-related genes. qPCR and immunofluorescence were used to evaluate the effects of JWC on H. pylori adhesion.Results: JWC showed considerable antibacterial activity against drug-resistant H. pylori strains, with minimum inhibitory concentration (MIC) values ranging from 64 to 1,024 μg/ml. The MIC of metronidazole (MTZ) against H. pylori 26,695–16R decreased from 64 to 6 μg/ml after treatment with 1/2 MIC of JWC. The resistance of H. pylori 26,695–16R to MTZ was reversed by JWC, and its effect was better than that of PaβN and CCCP. H. pylori 26,695–16R is a moderate biofilm-forming strain, and JWC (16–64 μg/ml) can inhibit the formation of biofilms in H. pylori 26,695–16R. JWC reduced the expression of HP0605-HP0607 (hefABC), HP0971-HP0969 (hefDEF), HP1327-HP1329 (hefGHI), and HP1489-HP1487. JWC reduced the adhesion of H. pylori to GES-1 cells and the expression of adhesives NapA, SabA, and BabA.Conclusion: The reversal of MTZ resistance by JWC may be achieved through the adhesin/efflux pump-biofilm pathway.
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International Journal of Electrochemical Science
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2023
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IF 1.5
Puji Peng,Feng Xu,Yuying Xu,Shuang Sun
This study presented the determination of Helicobacter pylori using a gold electrode (AuE)-based electrochemical biosensor in which the electroactive label was β-cyclodextrin (β-CD). The covalent immobilization of a thiol-decorated single-stranded DNA probe on the AuE surface occurred through the formation of a Au–S bond. The DNA hybridization was monitored via the differential pulse voltammetry (DPV) method, where the electrochemical signals for reduction of the β-CD bound to the double-stranded DNA (dsDNA) were measured. The electrochemical signal was linearly related to the target DNA concentration (0.3 nM–0.24 μM) when measured under optimal conditions, and the limit of detection (LOD) was determined to be as low as 0.15 nM, suggesting that measurements with our developed biosensor were highly repeatable and reproducible. In addition, our proposed biosensor was successfully applied to the determination of Helicobacter pylori in excrement.
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Micromachines
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2024
·Vol. 15
·期 3
·416
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IF 3
Hongzhuang Guo,Xiuyan Jin,Hao Zhang,Ping Gong,Xin Wang,Tingting Sun
In addressing the detection of drug resistance inHelicobacter pylori, we have successfully developed an efficient and highly accurate detection methodology. Initially, we designed and fabricated a microarray chip, which underwent finite element analysis for its optical and thermal characteristics. Ultimately, COC material was chosen as the processing material for the chip, ensuring superior performance. Subsequently, we established a comprehensive detection system and validated its performance. Following that, comparative experiments were conducted for detecting drug resistance inH. pylori. The experimental results indicate that our established methodology aligns with the results obtained using the E-test detection kit, achieving a concordance rate of 100%. In comparison to the E-test detection kit, our methodology reduces the detection time to 1.5 h and provides a more extensive coverage of detection sites.
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MICROCHEMICAL JOURNAL
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2026
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IF 5.2
Kun Zhao,Xin Gong,Qinglan Li,Jingyi,Mingxia Lin,Xiping Cui,Suqing Zhao
A nanozyme-amplified immunoassay was developed for Helicobacter pylori detection. • Avian-derived IgY and scFv enabled a dual-recognition sandwich format. • Porous PtCu nanozymes provided stable colorimetric signal amplification. • The assay achieved an LOD of 1.91 × 10 3 CFU/mL with good selectivity. • The method supports sensitive screening in matrix-rich samples. Helicobacter pylori ( H. pylori ) is a major gastric pathogen associated with chronic gastrointestinal diseases, creating a need for simple and reliable analytical methods for its detection, particularly in complex sample matrices. Herein, we developed a nanozyme-amplified colorimetric sandwich immunoassay by integrating a unified avian-derived dual-recognition format with porous PtCu nanozyme-based catalytic signal amplification. Egg yolk-derived immunoglobulin yolk (IgY) was used as the capture antibody, while a phage display-derived single-chain variable fragment (scFv) selected after chicken immunization and biopanning was assembled onto porous PtCu nanomicrobeads (PtCu NPMs) as the catalytic detection probe. This design combines complementary IgY/scFv recognition with the catalytic robustness of porous PtCu nanozyme for sensitive H. pylori detection. Under optimized conditions, the assay achieved a limit of detection of 1.91 × 10 3 CFU/mL and showed good selectivity toward H. pylori . The method was further evaluated in saliva, milk, water, and vegetable juice samples, where satisfactory recoveries were obtained at moderate-to-high spiking levels. These results indicate that the proposed assay is suitable for sensitive screening and semi-quantitative analysis of H. pylori in complex matrices, and provides a practical strategy for combining avian-derived recognition reagents with nanozyme-based signal amplification in pathogen detection. Scheme 1 . Schematic illustration of the PtCu NPMs@scFv-based nanozyme-amplified sandwich immunoassay for H. pylori detection. (A) Selection of avian-derived scFv against H. pylori by hen immunization and phage display. (B) Construction of the PtCu NPMs@scFv probe through electrostatic assembly on PtCu NPMs. (C) Proposed detection mechanism: egg-yolk-derived IgY captures H. pylori on the solid phase, scFv recognizes cell-surface antigenic determinants of H. pylori , and the resulting IgY H. pylori -PtCu NPMs@scFv sandwich complex enriches porous PtCu nanozyme at the interface, thereby catalyzing the TMB/H 2 O 2 reaction to generate an amplified colorimetric signal. Download: Download high-res image (153KB) Download: Download full-size image
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Advanced Science
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2026
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IF 14.1
Tianye Fang,Jinzhe Tong,Feng Feng,Cong Liu,Chang Shu,Jiaying Zhu,Shibo Zhang,Shuyue Deng,Wanchao Zuo,Yuhan Song,Jun Yang,Yanmin Ju,Yingying Xing,Jianjun Dai
Helicobacter pylori ( H. pylori ) is a leading cause of gastric cancer, but current antibiotic‐based therapies face challenges like low eradication rates, high recurrence, and intestinal flora disruption. Iron is critical for H. pylori ’s survival and pathogenicity, as the bacterium relies on maintaining iron homeostasis for normal proliferation, metabolism, and colonization of the stomach. Inspired by this, we propose a “nutritional trap” strategy, using bismuth as “fake iron” to trick the H. pylori ’s iron‐uptake system, triggering iron starvation. We then developed a bismuth‐based nanodrug (Bi‐TP@FU, TBF) modified with tea polyphenols and fucoidan for enhanced H. pylori targeting and gastric mucosal penetration. TBF targets and adheres to the surface of H. pylori by binding to the BabA protein, then induces iron starvation and metabolic disorders through competition between bismuth and iron, ultimately killing multidrug‐resistant strains without inducing resistance. Interestingly, TBF selectively eliminated pathogens while preserving probiotics, thus maintaining intestinal flora balance, which is superior to quadruple therapy. This novel oral TBF, which relies on a nutritional trap‐based bactericidal strategy, offers a new option for antibiotic alternative therapy of bacterial infections. A “nutritional trap” strategy centered on disrupting bacterial iron homeostasis is proposed. The synthesized Bi‐TP@FU (TBF) can target Helicobacter pylori , interfere with the bacterial iron uptake and utilization processes to disrupt its iron homeostasis, induce bacterial death, and meanwhile preserve the balance of the intestinal flora. This finding further offers a novel approach for antibiotic‐alternative therapies against Helicobacter pylori infection.
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Acta Pharmaceutica Sinica B
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2022
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IF 14.903
Xiaonan Chen,Yiqing Zou,Shuqi Zhang,Pengchao Fang,Shuxuan Li,Pengyu Li,Yingying Sun,Gang Yuan,Haiyan Hu
Helicobacter pylori ( H. pylori ), creating a global infection rate over 50%, presents great challenges in clinical therapies due to its complex pathological microenvironment in vivo . To improve the eradication efficacy, herein we fabricated a pharmaceutical vesicle RHL/Cl-Ch-cal where cholesterol-PEG, calcitriol and first-line antibiotic clarithromycin were co-loaded in the rhamnolipid-composed outer lipid layer. RHL/Cl-Ch-cal could quickly penetrate through gastric mucus layer to reach H. pylori infection sites, and then effectively destroyed the architecture of H. pylori biofilms, killed dispersed H. pylori and inhibited the re-adhesion of residual bacteria (called biofilms eradication tetralogy). Moreover, RHL/Cl-Ch-cal activated the host immune response to H. pylori by replenishing cholesterol to repair lipid raft on the cell membrane of host epithelial cells. Finally, RHL/Cl-Ch-cal killed the intracellular H. pylori through recovering the lysosomal acidification and assisting degradation. In experiments, RHL/Cl-Ch-cal demonstrated prominent anti- H. pylori efficacy in the classical H. pylori -infected mice model. Therefore, the study provides a “comprehensive attack” strategy for anti- H. pylori therapies including biofilms eradication tetralogy, immune activation and intracellular bacteria killing.
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ACS Applied Materials & Interfaces
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2022
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IF 10.383
Guiyun Deng,Yang Wu,Zhiyong Song,Shuojun Li,Moqing Du,Jiamin Deng,Quan Xu,Liu Deng,Hagar Shendy Bahlol,Heyou Han
Infection with Helicobacter pylori (Hp) is one of the leading causes of stomach cancer. The ability to treat Hp infection is hampered by a lack of stomach gastric acid environment. This work introduces a nanoliposome that can rapidly adjust the gastric acid environment to ensure a drug’s optimal efficacy. We introduce CaCO3@Fe–TP@EggPC nanoliposomes (CTE NLs) that are composed of Fe3+ and tea polyphenols (TPs) forming complexes on the surface of internal CaCO3 and then with lecithin producing a phospholipid bilayer on the polyphenols’ outer surface. Through the action of iron–TP chelate, the phospholipid layer can fuse with the bacterial membrane to eliminate Hp. Furthermore, CaCO3 can promptly consume the excessive gastric acid, ensuring an ideal operating environment for the chelate. TPs, on the other hand, can improve the inflammation and gut microbes in the body. The experimental results show that CTE NLs can quickly consume protons in the stomach and reduce the bacterial burden by 1.2 orders of magnitude while reducing the inflammatory factors in the body. The biosafety evaluation revealed that nanoliposomes have good biocompatibility and provide a new strategy for treating Hp infection.
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Food Bioscience
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2021
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IF 4.24
Fei Gao,Lin Sui,Guangqing Mu,Fang Qian,Xuemei Zhu
Helicobacter pylori is considered as the causative agent of gastrointestinal diseases. The large increase of drug-resistant strains caused by the treatment of H. pylori makes it very important to develop new treatment strategies. This study aimed to isolate and select Lactobacillus strains from infant feces and evaluate the inhibitory effects against H. pylori . Six strains were initially screened out of Forty-seven Lactobacillus strains obtained from healthy infants feces through evaluating acid (pH 3.0) and bile salt tolerance (0.3%). Based on the re-screening of the four indexes of transit tolerance, hydrophobicity , self-aggregation and anti- Helicobacter pylori , combined with the comprehensive evaluation of principal component analysis , these both strains of IF-3083 and IF-5014 were obtained. And these two strains were identified as Lactobacillus plantarum using 16S ribosomal RNA gene sequences. Also, the two identified strains showed good adhesion to human gastric adenocarcinoma (AGS) and human colorectal adenocarcinoma (HT-29) cells, γ-hemolytic activity and susceptibility to seven antibiotics. The viable count of H. pylori SS1 was significantly decreased when co-cultured with the live cells (LC) or cell-free supernatants (CFS) of these two strains. These preliminary results suggested that L. plantarum IF-3083 and L. plantarum IF-5014 had the potential to be used as probiotics to prevent H. pylori infection.
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Nature Communications
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2021
·Vol. 12
·期 1
·1-10
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IF 14.919
Zhang Lufeng,Zhang Liang,Deng Hui,Li Huan,Tang Wentao,Guan Luyao,Qiu Ye,Donovan Michael J.,Chen Zhuo,Tan Weihong
Helicobacter pylori infection is a major etiological factor in gastric diseases. However, clinical antibiotic therapy for H. pylori is limited by continuously decreased therapeutic efficacy and side effects to symbiotic bacteria. Herein, we develop an in vivo activatable pH-responsive graphitic nanozyme, PtCo@Graphene (PtCo@G), for selective treatment of H. pylori . Such nanozymes can resist gastric acid corrosion, exhibit oxidase-like activity to stably generate reactive oxygen species only in acidic gastric milieu and demonstrate superior selective bactericidal property. C 18 -PEG n -Benzeneboronic acid molecules are modified on PtCo@G, improving its targeting capability. Under acidic gastric pH, graphitic nanozymes show notable bactericidal activity toward H. pylori , while no bacterial killing is observed under intestinal conditions. In mouse model, high antibacterial capability toward H. pylori and negligible side effects toward normal tissues and symbiotic bacteria are achieved. Graphitic nanozyme displays the desired enzyme-like activities at corresponding physiological sites and may address critical issues in clinical treatment of H. pylori infections.
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BIOMATERIALS
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2016
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IF 8.387
Zi-Wei Jing,Yi-Yang Jia,Ning Wan,Min Luo,Meng-Lei Huan,Tai-Bin Kang,Si-Yuan Zhou,Bang-Le Zhang
The covalently modified ureido-conjugated chitosan/TPP multifunctional nanoparticles have been developed as targeted nanomedicine delivery system for eradication of Helicobacter pylori . H. pylori can specifically express the urea transport protein on its membrane to transport urea into cytoplasm for urease to produce ammonia, which protects the bacterium in the acid milieu of stomach. The clinical applicability of topical antimicrobial agent is needed to eradicate H. pylori in the infected fundal area. In this study, we designed and synthesized two ureido-conjugated chitosan derivatives UCCs-1 and UCCs-2 for preparation of multifunctional nanoparticles. The process was optimized in order to prepare UCCs/TPP nanoparticles for encapsulation of amoxicillin. The results showed that the amoxicillin-UCCs/TPP nanoparticles exhibited favorable pH-sensitive characteristics, which could procrastinate the release of amoxicillin at gastric acids and enable the drug to deliver and target to H. pylori at its survival region effectively. Compared with unmodified amoxicillin-chitosan/TPP nanoparticles, a more specific and effective H. pylori growth inhibition was observed for amoxicillin-UCCs/TPP nanoparticles. Drug uptake analysis tested by flow cytometry and confocal laser scanning microscopy verified that the uptake of FITC-UCCs-2/TPP nanoparticles was associated with urea transport protein on the membrane of H. pylori and reduced with the addition of urea as competitive transport substrate. These findings suggest that the multifunctional amoxicillin-loaded nanoparticles have great potential for effective therapy of H. pylori infection. They may also serve as pharmacologically effective nanocarriers for oral targeted delivery of other therapeutic drugs to treat H. pylori .
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IEEE SENSORS JOURNAL
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2024
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IF 4.3
Chen Ma,Dingnan Lu,Fangyuan Zhou,Jiayue Luo,Huihui Gan,Weidong He,Pradeep U. Kurup,David Z. Zhu
Due to the almost-complete dependence on clinical diagnosis, current Helicobacter pylori (H. pylori) epidemiological statistics suffer from fragmented geographical coverage and lagged data updating worldwide. Acquiring information based on the quantitative detection of biomarkers from domestic wastewater provides a promising way for the future H. pylori epidemiological study. Here, we report wastewater-adapted electrochemical competitive immunosensor (WECI). This method focuses explicitly on detecting H. pylori cytoplasmic ureB in wastewater and contains a series of designs to overcome the challenges brought by the complicated analytical matrix. The developed WECI achieved a practical detection range from 10 pg mL $^{-{1}}$ to 5.0 ng mL $^{-{1}}$ ( ${R}^{{2}}$ = 0.996) and showed the corresponding limit of detection (LoD) and limit of quantification (LoQ) of 0.37 and 1.4 pg mL $^{-{1}}$ , respectively. It can be prepared within 6 h and kept highly sensitive for at least six weeks. When testing real wastewater samples, WECI resulted in an average biomarkers recovery rate of 70.9%, which was remarkably higher than the average of 47.0% achieved using qPCR, indicating the excellent applicability toward actual wastewater detection. Our reported WECI is the first study to quantitatively detect H. pylori ureB from wastewater, opening up new vistas for H. pylori epidemiological study.
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Cell Death & Disease
·
2025
·Vol. 16
·期 1
·1-18
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IF 9.6
Lu Qiutong,Wang Zhaopeng,Cao Shuixian,Wang Huan,Li Nianshuang,Hu Yi,Ding Wuhui,Zuo Wei,Hong Junbo
Helicobacter pylori (H. pylori) infection is a significant cause of gastric diseases, with its pathogenic mechanisms still not fully understood. This study investigates the role of METTL3, an enzyme involved in m6A methylation, in modulating the CXCL1/NF-κB signaling pathway in H. pylori-induced gastritis. Using both bioinformatics analysis of GEO database and experimental approaches including MeRIP, RIP assays, and immunostaining, this research highlights how METTL3 influences CXCL1 expression and NF-κB pathway activation. Results from both in vitro and in vivo models show that METTL3 increases inflammatory responses and apoptosis in gastric cells. Suppression of METTL3 resulted in decreased inflammation and apoptosis, suggesting its potential as a therapeutic target in gastritis management.
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