Helicobacter pylori is a widespread bacterium that infects the stomach, causing gastric disorders associated with high morbidity and mortality worldwide. Current methods for identifying and quantifying this pathogen rely on invasive and non-invasive tests. Although combining these methods allows accurate diagnosis, they have multiple drawbacks, and there is no single reliable gold standard test. New, more sensitive strategies involving molecular techniques, such as digital PCR, have been developed but require complex and expensive instruments. Herein, we implement and validat a nanophotonic bimodal waveguide (BiMW) biosensor for the sensitive and accurate detection of H. pylori in gastric biopsies and stool. This biosensor offers real-time, label-free detection, high sensitivity, and the capability to be integrated into compact devices. By employing monoclonal antibodies targeting specific membrane proteins found in H. pylori, the biosensor enables unique recognition of the bacterium, demonstrating its potential as an alternative diagnostic tool. The BiMW biosensor provides highly accurate H. pylori quantification in under 20 min, with limits of detection (LOD) of 89 ± 35 CFU/mL for antrum gastric biopsies and 82 ± 9 CFU/mL for stool samples. Clinical validation with 40 samples (20 gastric biopsies and 20 stool samples) showed sensitivity and specificity of 90 % for gastric biopsies and 95 % for stool samples, offering diagnostic reliability equivalent to semiquantitative ELISA tests and enabling more efficient and timely detection of H. pylori infections. This test can significantly improve the speed of diagnosis and contribute to the development of more effective strategies for H. pylori eradication.

Helicobacter pylori (H. pylori), a microaerophilic gram-negative bacterium, is one of the most common chronic bacterial infections in humans, affecting about 50 % of the global population. Recently, it has been proposed that H. pylori infection might impact the efficacy of immune checkpoint inhibitors (ICIs), which are used in the treatment of various cancers, including gastric cancer (GC). However, the impact of H. pylori infection on clinical outcomes in patients with GC treated with ICIs is not yet fully elucidated.

Evaluating the impact of H. pylori infection status on overall survival (OS) and progression-free survival (PFS) on GC treated with ICIs.

A meticulous literature search was conducted across PubMed, EMBASE, and Web of Science databases, focusing on studies that compared the effect of H. pylori-positive status versus H. pylori-negative status on patients with GC undergoing ICI treatment. The Newcastle-Ottawa Scale was utilized for the risk of bias assessment of individual studies. For binary outcomes, we used hazard ratios (HRs) or odds ratios (OR) with 95 % confidence intervals (CI) to estimate the effect size.

In total, 3 studies were included, involving 928 patients, of which 396 had H. pylori-positive status. Analysis showed that: PFS was prolonged but not statistically significant in H. pylori-negative patients (HR: 1.11; 95 % CI:0.94-1.31; p = 0.17), OS was significantly prolonged in H. pylori-negative patients (HR: 1.25; 95 % CI: 1.05-1.50; p=0.012), and the H. pylori-negative group had a significant clinical response compared with the H. pylori-positive group (OR: 0.40; 95 % CI: 0.28-0.57; p < 0.000001).

In this systematic review and meta-analysis, the status of H. pylori provides a perspective to reshape ICI treatment paradigms and advocates for early eradication treatment of this bacterium.

The biofilm structure of Helicobacter pylori is known to enhance its capabilities for antimicrobial resistance. This study aims to investigate the role of the flagellar hook length control protein gene fliK in the biofilm formation of H. pylori. Homologous recombination was employed to knock out the fliK gene in the H. pylori NCTC 11637 strain. The flagella of H. pylori were observed using transmission electron microscopy (TEM), whereas H. pylori motility and growth were examined through semi-solid agar assays and growth curve analyses, respectively. The bacterial biofilm and its constituents were visualized utilizing fluorescence confocal microscopy. Assessments of H. pylori adhesion to gastric mucosal cells, its vacuolar toxicity, and antibiotic resistance were evaluated using co-culture experiments and E-test methods. The fliK gene was successfully knocked out in H. pylori NCTC 11637. The ΔfliK mutant exhibited polyhook structures or lacked typical flagellar morphology, reduced mobility, and a slower bacterial growth rate compared with the wild-type strain. Fluorescence confocal microscopy revealed a decrease in the thickness of the biofilm formed by the ΔfliK strain, along with reductions in polysaccharide and DNA components. The deletion of fliK did not affect vacuolar toxicity or antibiotic resistance but did reduce the adhesive capacity of the bacterium to gastric mucosal cells. The deletion of the fliK gene significantly impairs H. pylori biofilm formation, leading to substantial decreases in biofilm components, bacterial growth, and adhesion capabilities. These findings underscore the importance of fliK in the pathogenicity of H. pylori.IMPORTANCEThe increasing antibiotic resistance of Helicobacter pylori has emerged as a global health concern, with biofilm formation serving as a crucial mechanism underlying this resistance. This study investigates the role of the fliK gene, which encodes the flagellar hook length control protein, in H. pylori biofilm formation. Furthermore, we examined the influence of fliK on H. pylori growth, motility, and cellular adhesion capabilities. Our findings elucidate the molecular mechanisms governing H. pylori biofilm formation and suggest potential therapeutic strategies for addressing H. pylori antibiotic resistance.

Helicobacter pylori (H. pylori) is prevalent in over 50% of the global population and is recognized as the primary etiological agent for the development of gastric cancer. With the increasing incidence of antibiotic resistance, clinical treatment of H. pylori is a significant challenge. The formation of H. pylori biofilm is an important reason for antibiotic resistance and chronic infection, and it is also one of the key obstacles to eradicating H. pylori. H. pylori biofilm acts as a physical barrier, preventing the penetration of antibiotics and increasing the expression of efflux pump genes and drug-resistant gene mutations. Therefore, the treatment of H. pylori biofilm is extremely challenging. Nanomaterials, such as inorganic nanoparticles, lipid-based nanoparticles, and polymeric nanoparticles, which have properties including disrupting bacterial cell membranes, controlling drug release, and overcoming antibiotic resistance, have attracted significant interest. Furthermore, nanomaterials have the ability to treat H. pylori biofilm owing to their unique size, structure, and physical properties, including the inhibition of biofilm formation, enhancement of biofilm permeability, and disruption of mature biofilm. Moreover, nanomaterials have targeting functions and can carry antimicrobial drugs that play a synergistic role, thus providing a prospective strategy for treating H. pylori biofilm. In this review, we summarize the formation and antibiotic-resistance mechanisms of H. pylori biofilm and outline the latest progress in nanomaterials against H. pylori biofilm with the aim of laying the foundation for the development and clinical application of nanomaterials for anti-H. pylori biofilm.

Helicobacter pylori (H. pylori) infection is an important global public health concern, causing conditions like gastritis, gastroduodenal ulcers, gastric lymphoma, distal gastric cancer and other gastric diseases. With the increasing prevalence of antibiotics resistance, the cure rate of antibiotics-based triple or quadruple therapy has declined to 80 % or less. Moreover, side effects still remain. Hence, alternative, more potent and safer anti-H. pylori medications are required. Numerous studies have indicated that natural products from medical plants are valuable repositories for the prevention of H. pylori infection with advantages in little side effects due to the co-evolution with biological systems for millions of years. In this review, we highlighted the anti-H. pylori activities and the responsive mechanism of edible and medical plants based on epidemiological, experimental, and clinical studies, providing the basis for future development of functional foods or drugs against H. pylori.

The genes that encode the universal stress protein (USP) family domain (pfam00582) aid the survival of bacteria in specific host or habitat-induced stress conditions. Genome sequencing revealed that the genome of Helicobacter pylori, a gastric cancer pathogen, typically contains one USP gene, while related helicobacters have one or two distinct USP genes. However, insights into the functions of Helicobacteraceae (Helicobacter and Wolinella) USP genes are still limited to inferences from large-scale genome sequencing. Thus, we have combined bioinformatics and visual analytics approaches to conduct a more comprehensive data investigation of a set of 1045 universal stress protein sequences encoded in 1014 genomes including 785 Helicobacter pylori genomes. The study generated a representative set of 183 USP sequences consisting of 180 Helicobacter sequences, two Wolinella succinogenes sequences, and a sequence from a related campylobacteria. We used the amino acid residues and positions of the 12 possible functional sites in 1030 sequences to identify 25 functional sites patterns for guiding studies on functional interactions of Helicobacteraceae USPs with ATP and other molecules. Genomic context searches and analysis identified USP genes of gastric and enterohepatic helicobacters that are adjacent or in operons with genes for proteins responsive to DNA-damaging oxidative stress (ATP-dependent proteases: ClpS and ClpA); and DNA uptake proteins (natural competence for transformation proteins: ComB6, ComB7, ComB8, ComB9, ComB10, ComBE, and conjugative transfer signal peptidase TraF). Since transcriptomic evidence indicates that oxidative stress and the presence of virulence-associated genes regulate the transcription of H. pylori USP gene, we recommend further research on Helicobacter USP genes and their neighboring genes in oxidative stress response and virulence of helicobacters. To facilitate the reuse of data and research, we produced interactive analytics resources of a dataset composed of values for variables including phylogeography of H. pylori strains, protein sequence features, and gene neighborhood.

Flagella-mediated swarming motility plays a crucial role in facilitating the rapid colonization and dissemination of bacterial within the host. The swarming motility of Pseudomonas plecoglossicida is intricately associated with its lateral flagella, and notably, the lateral flagella system of P. plecoglossicida encompasses a transcriptional regulator known as LafK. However, the regulatory role of LafK and its impact on bacteria-host interactions remain to be elucidated. In this study, we systematically investigated the regulatory role of LafK by constructing lafK deletion strain on the biological characteristics, virulence, and pathogenic process of P. plecoglossicida, as well as its impact on the host immune response. Our findings demonstrated that the deletion of lafK led to a significant down-regulation in the expression of type III secretion system-associated genes within the lateral flagella of P. plecoglossicida, consequently impairing bacterial swarming motility, biofilm formation, adhesion, and chemotaxis ability. Furthermore, in vitro infection experiments demonstrated that the deletion of lafK resulted in a diminished pathogenicity of P. plecoglossicida through down-regulation of flagella-related genes, thereby triggering an expedited immune response for bacterial clearance, and subsequently leading to reduced bacterial load within the host and attenuated tissue damage during infection. In summary, this study presents a novel theoretical framework for elucidating the regulatory mechanism of virulence in P. plecoglossicida.

Gastric cancer remains a significant global health challenge, with Helicobacter pylori (H. pylori) recognized as a major etiological agent, affecting an estimated 50% of the world's population. There has been a rapidly expanding knowledge of the molecular and pathogenetic mechanisms of H. pylori over the decades. This review summarizes the latest research advances to elucidate the molecular mechanisms underlying the H. pylori infection in gastric carcinogenesis. Our investigation of the molecular mechanisms reveals a complex network involving STAT3, NF-κB, Hippo, and Wnt/β-catenin pathways, which are dysregulated in gastric cancer caused by H. pylori. Furthermore, we highlight the role of H. pylori in inducing oxidative stress, DNA damage, chronic inflammation, and cell apoptosis-key cellular events that pave the way for carcinogenesis. Emerging evidence also suggests the effect of H. pylori on the tumor microenvironment and its possible implications for cancer immunotherapy. This review synthesizes the current knowledge and identifies gaps that warrant further investigation. Despite the progress in our previous knowledge of the development in H. pylori-induced gastric cancer, a comprehensive investigation of H. pylori's role in gastric cancer is crucial for the advancement of prevention and treatment strategies. By elucidating these mechanisms, we aim to provide a more in-depth insights for the study and prevention of H. pylori-related gastric cancer.

Helicobacter pylori ( H. Pylori ) is considered a main causative organism of gastric ulcers, gastric cancer and duodenal ulcers. The current treatment relies on a combination of antimicrobial agents and acid suppressant agents, but the eradication effect is not satisfactory. To clarify the concentration of antibiotics at the lesion site, we investigate the clinical efficacy and drug tissue distribution of the combination therapy of furazolidone and tetracycline in eradicating H. Pylori.

Patients with H. pylori infection (n = 60) were randomized to either group A or B. Bismuth potassium citrate capsules 220 mg, omeprazole enteric-coated capsules 20 mg, amoxicillin capsules 1000 mg, each twice per day, and furazolidone tablets 500 mg were administered to group A. Group B was treated with bismuth potassium citrate capsules 220 mg, omeprazole enteric-coated capsules 20 mg, amoxicillin capsules 1000 mg, and tetracycline tablets 500 mg each twice per day for 2 weeks. The serum and gastric juice, gastric antrum, gastric horn, and gastric body samples were taken under a gastroscope on the 14th day. The antimicrobial concentrations in serum and tissue samples were determined by high-performance liquid chromatography.

In the negative group of furazolidone, the concentrations of gastric antrum, gastric body, and gastric angle were significantly higher than those in the positive group ( P = 0.017, 0.015, and 0.028). The concentrations of furazolidone in gastric fluid, gastric antrum, gastric angle, and gastric body were ∼421 times, 82 times, 17 times, and 51 times higher than those in serum, respectively. The concentrations of tetracycline in the serum and gastric angle of the tetracycline negative group were significantly higher than those in the positive group ( P = 0.036 and 0.042), and the tetracycline concentrations in the gastric horn and gastric body were about 4 and 6 times higher than those in the serum, respectively. The concentration of amoxicillin in group B was higher than that in group A, especially in serum, gastric juice, gastric angle, and gastric body ( P < 0.05).

Furazolidone is mainly concentrated and sequentially distributed in gastric juice, gastric antrum, and gastric body tissue, and tetracycline is mainly distributed in serum, gastric angle, and gastric body, whereas amoxicillin is mainly distributed in serum, gastric juice, gastric angle, and gastric body. Improving the concentration and tissue distribution of antibacterial drugs in the human gastric mucosa is the key to ensuring the ideal eradication rate of quadruple therapy.

Helicobacter pylori (H. pylori) is closely associated with gastric cancer and peptic ulcers. The effectiveness of antibiotic treatment against H. pylori is diminished by the emergence of drug-resistant strains, side effects, high cost and reinfections. Given the circumstances, it is imperative to develop a potent vaccination targeting H. pylori. Understanding H. pylori's pathogenicity and the host's immune response is essential to developing a vaccine. Furthermore, vaccine evaluation necessitates the careful selection of design formulation. This review article aims to provide a concise overview of the considerations involved in selecting the optimal antigen, adjuvant, vaccine delivery system and laboratory animal model for vaccine formulation. Furthermore, we will discuss some significant obstacles in the realm of developing a potent vaccination against H. pylori.

Obesity and diabetes mellitus (DM) have become public health concerns worldwide. Both conditions have severe consequences and are associated with significant medical costs and productivity loss. Additionally, Helicobacter pylori infection may be a risk factor for the development of these conditions. However, whether eradicating H. pylori infection directly causes weight loss or improves insulin sensitivity is unknown.

In this study, we confirmed the effect of sleeve gastrectomy according to the state of the gastric microbiota in 40 patients with obesity, DM, and H. pylori infection. Patients with obesity were divided into four groups: non-DM without H. pylori infection (ND), non-DM with H. pylori infection (ND-HP), DM, and DM with H. pylori infection (DM-HP) using 16S V3-V4 sequencing.

In the DM group, ALT, hemoglobin, HbA1c, blood glucose, and HSI significantly decreased, whereas high-density lipoprotein significantly increased. However, in the H. pylori-positive group, no significant difference was observed. The diversity of gastric microbiota decreased in the order of the ND > DM > ND-HP > DM-HP groups. We also conducted a correlation analysis between the preoperative microbes and clinical data. In the ND-HP group, most of the top 20 gastric microbiota were negatively correlated with glucose metabolism. However, H. pylori infection was positively correlated with pre-insulin levels.

Therefore, these findings indicate that patients with obesity and diabetes clearly benefit from surgery, but H. pylori infection may also affect clinical improvement.

Biofilm formation in Helicobacter pylori (H. pylori) helps bacteria survive antibiotic exposure and supports bacterial colonization and persistence in the stomach. Most of the published articles have focused on one aspect of the biofilm. Therefore, we conducted the current study to better understand the mechanism of biofilm formation, how the biofilm contributes to antibiotic resistance, and how the biofilm modifies the medication delivery mechanism.

We conducted a literature review analysis of the published articles on the Helicobacter pylori biofilm between 1998 and 2024 from the PubMed database to retrieve eligible articles. After applying the inclusion and exclusion criteria, two hundred and seventy-three articles were eligible for our study.

The results showed that biofilm formation starts as adhesion and progresses through micro-colonies, maturation, and dispersion in a planktonic form. Moreover, specific genes modulate each phase of biofilm formation. Few studies have shown that mechanisms, such as quorum sensing and diffusible signal factors, enhance coordination among bacteria when switching from biofilm to planktonic states. Different protein expressions were also observed between planktonic and biofilm strains, and the biofilm architecture was supported by exopolysaccharides, extracellular DNA, and outer membrane vesicles.

This infrastructure is responsible for the increased survival of bacteria, especially in harsh environments or in the presence of antibiotics. Therefore, understanding the biofilm formation for H. pylori is crucial. This study illustrates biofilm formation in H. pylori to help improve the treatment of H. pylori infection.

Stutzerimonas nitrititolerans (S. nitrititolerans) is a rare human pathogenic bacterium and has been inadequately explored at the genomic level. Here, we report the first case of carbapenem-resistant S. nitrititolerans isolated from the peritoneal dialysis fluid of a patient with chronic renal failure. This study analyzed the genomic features, antimicrobial resistance, and virulence factors of the isolated strain through whole genome sequencing (WGS).

The bacterial isolate from the peritoneal dialysis fluid was named PDI170223, and preliminary identification was conducted through Matrix-assisted laser desorption ionization/time of flight mass spectrometry (MALDI-TOF MS). WGS of the strain PDI170223 was performed using the Illumina platform, and a phylogenetic tree was constructed based on the 16S rRNA gene sequences. Antimicrobial susceptibility test (AST) was conducted using the TDR-200B2 automatic bacteria identification/drug sensitivity tester.

S. nitrititolerans may emerge as a human pathogen due to its numerous virulence genes, including those encoding toxins, and those involved in flagellum and biofilm formation. The AST results revealed that the strain is multidrug- and carbapenem-resistant. The antimicrobial resistance genes of S. nitrititolerans are complex and diverse, including efflux pump genes and β⁃lactam resistance genes.

The analysis of virulence factors and antimicrobial resistance of S. nitrititolerans provides clinical insight into the pathogenicity and potential risks of this bacterium. It is crucial to explore the mechanisms through which S. nitrititolerans causes diseases and maintains its antimicrobial resistance, thereby contributing to development of effective treatment and prevention strategies.

A wealth of research indicates that superficial gastritis (SG) and atrophic gastritis (AG) are precursors to gastric cancer (GC). While Helicobacter pylori (H. pylori) has long been recognized as a key player in GC development, recent findings by Fu et al. have identified Streptococcus anginosus (S. anginosus) as an emerging pathogen that can trigger SG, AG and GC. S. anginosus, a gram-positive coccus, leverages its surface protein T. pallidum membrane protein C (TMPC) to engage with the annexin A2 (ANXA2) receptor of gastric epithelial cells, facilitating its colonization and invasion in the gastric mucosa. This leads to an upregulation of proinflammatory chemokines Ccl20 and Ccl8, causing prolonged effects on gastric barrier function and microbiota homeostasis, leading to SG. Moreover, these bacteria activate the mitogen-activated protein kinase (MAPK) signaling pathway, which is associated with the development of AG and GC. Importantly, inhibiting TMPC or knocking down ANXA2 can reduce S. anginosus colonization and invasion, lowering the chances of SG, AG, and GC. This paper highlights the molecular mechanisms of S. anginosus in SG, AG and GC, emphasizing the importance of a multi-pathogen strategy in gastric disease management and the need for further investigation into the role of S. anginosus in GC progression.

Helicobacter pylori is a gram-negative, spiral-shaped, flagellated bacterium that colonizes the stomach of half the world's population. Helicobacter pylori infection causes pathologies of varying severity. Standard oral therapy fails in 15-20% since the barriers of the oral route decrease the bioavailability of antibiotics and the intrinsic factors of bacteria increase the rates of resistance. Nanoparticles and microparticles are promising strategies for drug delivery into the gastric mucosa and targeting H. pylori. The variety of building blocks creates systems with distinct colloidal, surface, and biological properties. These features improve drug-pathogen interactions, eliminate drug depletion and overuse, and enable the association of multiple actives combating H. pylori on several fronts. Nanoparticles and microparticles are successfully used to overcome the barriers of the oral route, physicochemical inconveniences, and lack of selectivity of current therapy. They have proven efficient in employing promising anti-H. pylori compounds whose limitation is oral route instability, such as some antibiotics and natural products. However, the current challenge is the applicability of these strategies in clinical practice. For this reason, strategies employing a rational design are necessary, including in the development of nano- and microsystems for the oral route.

Clarithromycin (CLR) is currently a key antibiotic for Helicobacter pylori infection treatment, however, the data on CLR resistance patterns in Russia are missing. Here, we applied WGS-based approach to H. pylori clinical isolates from Russia to comprehensively investigate sequence variation, identify putative markers of CLR resistance and correlate them with phenotypic susceptibility testing. The phenotypic susceptibility of 44 H. pylori isolates (2014-2022) to CLR was determined by disc diffusion method: 23 isolates were CLR-resistant and 21-CLR-susceptible. All isolates were subjected to WGS and submitted to GenBank. Based on complete sequence analysis, we showed that among all sequence variants, the combination of mutations A2146G/A2147G in the 23S rRNA gene is the most reliable for prediction of phenotypic susceptibility. For the first time, the average number of mutations in 106 virulence-associated genes between resistant and susceptible groups were compared. Moreover, this study presents the first WGS insight into genetic diversity of H. pylori in Russia with a particular focus on the molecular basis of drug resistance: the novel mutations were described as potential markers for the resistance development. Of these, the most prominent was a frameshift deletion (252:CGGGT) in HP0820 coding region, which is a good candidate for further investigation.

Cinnamomum cassia Presl (Cinnamomum cassia) is a common traditional Chinese medicine, which can promote the secretion and digestion of gastric juice, improve the function of gastrointestinal tract. Cinnamaldehyde (CA) is a synthetic food flavoring in the Chinese Pharmacopoeia.

This study aimed to search for the active ingredient (CA) of inhibiting H. pylori from Cinnamomum cassia, and elucidate mechanism of action, so as to provide the experimental basis for the treatment of H. pylori infection with Cinnamomum cassia.

It's in vitro and in vivo pharmacological properties were evaluated based on minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), and an acute gastric inflammation model in mice infected with H. pylori. Drug safety was evaluated using the CCK8 method and high-dose administration in mice. The advantageous characteristics of CA in inhibiting H. pylori were confirmed using acidic conditions and in combination with the antibiotics. The mechanism underlying the action of CA on H. pylori was explored using scanning electron microscopy (SEM), adhesion experiments, biofilm inhibition tests, ATP and ROS release experiments, and drug affinity responsive target stability (DARTS) screening of target proteins. The protein function and target genes were verified by molecular docking and Real-Time quantitative reverse transcription PCR (qRT-PCR).

The results demonstrated that CA was found to be the main active ingredient against H. pylori in Cinnamomum cassia in-vitro tests, with a MIC of 8-16 μg/mL. Moreover, CA effectively inhibited both sensitive and resistant H. pylori strains. The dual therapy of PPI + CA exhibited remarkable in vivo efficacy in the acute gastritis mouse model, superior to the standard triple therapy. DARTS, molecular docking, and qRT-PCR results suggested that the target sites of action were closely associated with GyrA, GyrB, AtpA, and TopA, which made DNA replication and transcription impossible, then leading to inhibition of bacterial adhesion and colonization, suppression of biofilm formation, and inhibition ATP and enhancing ROS.

This study demonstrated the suitability of CA as a promising lead drug against H. pylori, The main mechanisms can target GyrA ect, leading to reduce ATP and produce ROS, which induces the apoptosis of bacterial.

This letter considers the possibility of using the optical trap to study the structure and function of the microbial flagellum. The structure of the flagellum of a typical gram-negative bacterium is described in brief. A standard mathematical model based on the principle of superposition is used to describe the movement of an ellipsoidal microbial cell in a liquid medium. The basic principles of optical trapping based on the combined action of the light pressure and the gradient force are briefly clarified. Several problems related to thermal damage of living microscopic objects when the latter gets to the focus of a laser beam are shortly discussed. It is shown that the probability of cell damage depends nonlinearly on the wavelength of laser radiation. Finally, the model systems that would make it possible to study flagella of the free bacteria and the ones anchored or tethered on the surface of a solid material are discussed in detail.

Cancers associated with pathogen infections are gradually becoming important threats to human health globally, and it is of great significance to study the mechanisms of pathogen carcinogenesis. Current mechanistic studies rely on animal and two-dimensional (2D) cell culture models, but traditional methods have been proven insufficient for the rapid modeling of diseases caused by new pathogens. Therefore, research focus has shifted to organoid models, which can replicate the structural and genetic characteristics of the target tissues or organs in vitro, providing new platforms for the study of pathogen-induced oncogenic mechanisms. This review summarizes the application of organoid technology in the studies of four pathogen-associated cancers: gastric cancer linked to Helicobacter pylori, liver cancer associated with hepatitis B virus or hepatitis C virus, colorectal cancer caused by Escherichia coli, and cervical cancer related to human papillomavirus. This review also proposes several limitations of organoid technology to optimize organoid models and advance the treatment of cancer associated with pathogen infections in the future.

Helicobacter pylori infection causes chronic gastritis, ulcers, and gastric cancer, making it a threat to human health. Despite the use of antibiotic therapy, the global prevalence of H. pylori infection remains high, necessitating early eradication measures. Immunotherapy, especially vaccine development, is a promising solution in this direction, albeit the selection of an appropriate animal model is critical in efficient vaccine production. Accordingly, we conducted a literature, search and summarized the commonly used H. pylori strains, H. pylori infection-related animal models, and models for evaluating H. pylori vaccines. Based on factors such as the ability to replicate human diseases, strain compatibility, vaccine types, and eliciting of immune responses, we systematically compared the advantages and disadvantages of different animal models, to obtain the informed recommendations. In addition, we have proposed novel perspectives on H. pylori-related animal models to advance research and vaccine evaluation for the prevention and treatment of diseases such as gastric cancer.

BACKGROUND Helicobacter pylori has a high infection rate worldwide, and epidemiological study of H. pylori is important. Artificial intelligence has been widely used in the field of medical research and has become a hotspot in recent years. This paper proposed a prediction model for H. pylori infection based on machine learning in adults. MATERIAL AND METHODS Adult patients were selected as research participants, and information on 30 factors was collected. The chi-square test, mutual information, ReliefF, and information gain were used to screen the feature factors and establish 2 subsets. We constructed an H. pylori infection prediction model based on XGBoost and optimized the model using a grid search by analyzing the correlation between features. The performance of the model was assessed by comparing its accuracy, recall, precision, F1 score, and AUC with those of 4 other classical machine learning methods. RESULTS The model performed better on the part B subset than on the part A subset. Compared with the other 4 machine learning methods, the model had the highest accuracy, recall, F1 score, and AUC. SHAP was used to evaluate the importance of features in the model. It was found that H. pylori infection of family members, living in rural areas, poor washing hands before meals and after using the toilet were risk factors for H. pylori infection. CONCLUSIONS The model proposed in this paper is superior to other models in predicting H. pylori infection and can provide a scientific basis for identifying the population susceptible to H. pylori and preventing H. pylori infection.

Helicobacter pylori is a gastric oncopathogen that infects over half of the world's human population. It is a Gram-negative, microaerophilic, helix-shaped bacterium that is equipped with flagella, which provide high motility. Colonization of the stomach is asymptomatic in up to 90% of people but is a recognized risk factor for developing various gastric disorders such as gastric ulcers, gastric cancer and gastritis. Invasion of the human stomach occurs via numerous virulence factors such as CagA and VacA. Similarly, outer membrane proteins (OMPs) play an important role in H. pylori pathogenicity as a means to adapt to the epithelial environment and thereby facilitate infection. While some OMPs are porins, others are adhesins. The epithelial cell receptors SabA, BabA, AlpA, OipA, HopQ and HopZ have been extensively researched to evaluate their epidemiology, structure, role and genes. Moreover, numerous studies have been performed to seek to understand the complex relationship between these factors and gastric diseases. Associations exist between different H. pylori virulence factors, the co-expression of which appears to boost the pathogenicity of the bacterium. Improved knowledge of OMPs is a major step towards combatting this global disease. Here, we provide a current overview of different H. pylori OMPs and discuss their pathogenicity, epidemiology and correlation with various gastric diseases.

Background: Helicobacter pylori is implicated in the development of gastritis, ulcers, and various gastric cancers, representing significant morbidity, mortality, and healthcare spending. Patients with H. pylori infection have traditionally been treated with oral antibiotics, however, oral therapy is not feasible in all clinical situations. We examined the available evidence supporting the use of intravenous (IV) antibiotics in H. pylori. Methods: This systematic review was carried out by reviewing multiple electronic databases: MEDLINE, CENTRAL, EMBASE, CINAHL, Clinicaltrials.org, and the World Health Organization (WHO) database of clinical trials. Articles published from database inception until February 12, 2023 that discussed the use of IV antibiotics in H. pylori management were included. Results: The search strategy identified 978 studies, with 11 meeting the inclusion criteria. The results demonstrate that there is a lack of robust trials examining the use of IV antibiotics in H. pylori management. Many trials demonstrated that IV antibiotics were safe and efficacious but the results are limited by inconsistencies in the year and geographic location trials were conducted, the IV and oral antibiotic regimens, and the duration of therapy. Conclusions: IV antibiotics appear to be a feasible therapeutic alternative in the management of H. pylori and can be considered, especially in patient populations where oral therapy is contraindicated.

This study aims to comprehensively review the multifaceted factors underlying the successful colonization and infection process of Helicobacter pylori (H. pylori), a prominent Gram-negative pathogen in humans. The focus is on elucidating the functions, mechanisms, genetic regulation, and potential cross-interactions of these elements.

Employing a literature review approach, this study examines the intricate interactions between H. pylori and its host. It delves into virulence factors like VacA, CagA, DupA, Urease, along with phase variable genes, such as babA, babC, hopZ, etc., giving insights about the bacterial perspective of the infection The association of these factors with the infection has also been added in the form of statistical data via Funnel and Forest plots, citing the potential of the virulence and also adding an aspect of geographical biasness to the virulence factors. The biochemical characteristics and clinical relevance of these factors and their effects on host cells are individually examined, both comprehensively and statistically.

H. pylori is a Gram-negative, spiral bacterium that successfully colonises the stomach of more than half of the world's population, causing peptic ulcers, gastric cancer, MALT lymphoma, and other gastro-duodenal disorders. The clinical outcomes of H. pylori infection are influenced by a complex interplay between virulence factors and phase variable genes produced by the infecting strain and the host genetic background. A meta-analysis of the prevalence of all the major virulence factors has also been appended.

This study illuminates the diverse elements contributing to H. pylori's colonization and infection. The interplay between virulence factors, phase variable genes, and host genetics determines the outcome of the infection. Despite biochemical insights into many factors, their comprehensive regulation remains an understudied area. By offering a panoramic view of these factors and their functions, this study enhances understanding of the bacterium's perspective, i.e. H. pylori's journey from infiltration to successful establishment within the host's stomach.

Helicobacter pylori (H. pylori), known for causing gastric inflammation, gastritis and gastric cancer, prompted our study to investigate the differential expression of cytokines in gastric tissues, which is crucial for understanding H. pylori infection and its potential progression to gastric cancer. Focusing on Il-1β, IL-6, IL-8, IL-12, IL-18, and TNF-α, we analysed gene and protein levels to differentiate between H. pylori-infected and non-infected gastritis. We utilised real-time quantitative polymerase chain reaction (RT-qPCR) for gene quantification, immunohistochemical staining, and ELISA for protein measurement. Gastric samples from patients with gastritis were divided into three groups: (1) non-gastritis (N-group) group, (2) gastritis without H. pylori infection (G-group), and (3) gastritis with H. pylori infection (GH-group), each consisting of 8 samples. Our findings revealed a statistically significant variation in cytokine expression. Generally, cytokine levels were higher in gastritis, but in H. pylori-infected gastritis, IL-1β, IL-6, and IL-8 levels were lower compared to H. pylori-independent gastritis, while IL-12, IL-18, and TNF-α levels were higher. This distinct cytokine expression pattern in H. pylori-infected gastritis underscores a unique inflammatory response, providing deeper insights into its pathogenesis.

Helicobacter pylori infection is widely spread globally and is known to cause potentially serious diseases. Several diagnostic methods exist to identify and treat carriers of this bacterium. Serological tests for the diagnosis of infection are based on the detection of antibodies immunoglobulin G against H. pylori, a non-invasive, inexpensive, and easy-to-perform option.

This research aims to ascertain the accuracy of an immunochromatographic serological test to verify the feasibility of using this method in patients who have not undergone previous eradication therapy.

Rapid tests and questionnaires were applied to 53 patients that underwent upper digestive endoscopy with research for H. pylori between the period of September and October 2021. The results were compared with histopathology.

In the rapid tests, seven positive and 46 negative results were obtained. When compared with the gold stan-dard, the following values were described: sensitivity 54.5%, specificity 97.6%, positive predictive value 85.7%, and negative predictive value 89.1%.

In the present study, the immunochromatographic serological tests had an accuracy close to the values found in other similar studies. Therefore, it may be concluded that the rapid serological test remains a reasonable choice for screening large populations due to its low cost and ease of application, especially in those individuals who have not undergone previous treatment.

• Helicobacter pylori infection can cause potentially serious diseases.

• Serological tests are based on the detection of antibodies immunoglobulin G against Helicobacter pylori.

• Serological tests for the diagnosis of Helicobacter pylori infection are low cost tools and have easy application.

• Rapid serological test is a reasonable choice for screening large populations.

The challenge facing Helicobacter pylori (H. pylori) infection management in some parts of Africa is the evolution of drug-resistant species, the lack of gold standard in diagnostic methods, and the ineffectiveness of current vaccines against the bacteria. It is being established that even though clinical consequences linked to the bacteria vary geographically, there is rather a generic approach to treatment. This situation has remained problematic in the successful fight against the bacteria in parts of Africa. As a result, this study compared the genomes of selected H. pylori isolates from selected areas of Africa and evaluated their virulence and antibiotic drug resistance, those that are highly pathogenic and are associated with specific clinical outcomes and those that are less virulent and rarely associated with clinical outcomes. 146 genomes of H. pylori isolated from selected locations of Africa were sampled, and bioinformatic tools such as Abricate, CARD RGI, MLST, Prokka, Roary, Phandango, Google Sheets, and iTOLS were used to compare the isolates and their antibiotic resistance or susceptibility. Over 20 k virulence and AMR genes were observed. About 95% of the isolates were genetically diverse, 90% of the isolates harbored shell genes, and 50% harbored cloud and core genes. Some isolates did not retain the cagA and vacA genes. Clarithromycin, metronidazole, amoxicillin, and tinidazole were resistant to most AMR genes (vacA, cagA, oip, and bab). Conclusion. This study found both virulence and AMR genes in all H. pylori strains in all the selected geographies around Africa with differing quantities. MLST, Pangenome, and ORF analyses showed disparities among the isolates. This in general could imply diversities in terms of genetics, evolution, and protein production. Therefore, generic administration of antibiotics such as clarithromycin, amoxicillin, and erythromycin as treatment methods in the African subregion could be contributing to the spread of the bacterium's antibiotic resistance.

Helicobacter pylori (H. pylori) is the predominant pathogen causing chronic gastric mucosal infections globally. During the period from 2011 to 2022, the global prevalence of H. pylori infection was estimated at 43.1%, while in China, it was slightly higher at approximately 44.2%. Persistent colonization by H. pylori can lead to gastritis, peptic ulcers, and malignancies such as mucosa-associated lymphoid tissue (MALT) lymphomas and gastric adenocarcinomas. Despite eliciting robust immune responses from the host, H. pylori thrives in the gastric mucosa by modulating host immunity, particularly by altering the functions of innate and adaptive immune cells, and dampening inflammatory responses adverse to its survival, posing challenges to clinical management. The interaction between H. pylori and host immune defenses is intricate, involving evasion of host recognition by modifying surface molecules, manipulating macrophage functionality, and modulating T cell responses to evade immune surveillance. This review analyzes the immunopathogenic and immune evasion mechanisms of H. pylori, underscoring the importance of identifying new therapeutic targets and developing effective treatment strategies, and discusses how the development of vaccines against H. pylori offers new hope for eradicating such infections.

In bacterial flagellum biogenesis, secretion of the hook-filament junction proteins FlgK and FlgL and completion of the flagellum requires the FlgN chaperone. Similarly, the related FliT chaperone is necessary for the secretion of the filament cap protein FliD and binds the flagellar export gate protein FlhA and the flagellum ATPase FliI. FlgN and FliT require FliJ for effective substrate secretion. In Helicobacter pylori, neither FlgN, FliT, nor FliJ have been annotated. We demonstrate that the genome location of HP1120 is identical to that of flgN in other flagellated bacteria and that HP1120 is the homolog of Campylobacter jejuni FlgN. A modeled HP1120 structure contains three α-helices and resembles the FliT chaperone, sharing a similar substrate-binding pocket. Using pulldowns and thermophoresis, we show that both HP1120 and a HP1120Δ126-144 deletion mutant bind to FlgK with nanomolar affinity, but not to the filament cap protein FliD, confirming that HP1120 is FlgN. Based on size-exclusion chromatography and multi-angle light scattering, H. pylori FlgN binds to FlgK with 1:1 stoichiometry. Overall structural similarities between FlgN and FliT suggest that substrate recognition on FlgN primarily involves an antiparallel coiled-coil interface between the third helix of FlgN and the C-terminal helix of the substrate. A FlgNΔ126-144 N100A, Y103A, S111I triple mutant targeting this interface significantly impairs the binding of FlgK. Finally, we demonstrate that FlgNΔ126-144 , like FliT, binds with sub-micromolar affinity to the flagellum ATPase FliI or its N-terminal domain. Hence FlgN and FliT likely couple delivery of low-abundance export substrates to the flagellum ATPase FliI.

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the gastric mucosa and is associated with various gastrointestinal disorders. H. pylori is a pervasive pathogen, infecting nearly 50% of the world's population, and presents a substantial concern due to its link with gastric cancer, ranking as the third most common cause of global cancer-related mortality. This review article provides an updated and comprehensive overview of the current understanding of H. pylori infection, focusing on its pathogenesis, diagnosis, and treatment strategies. The intricate mechanisms underlying its pathogenesis, including the virulence factors and host interactions, are discussed in detail. The diagnostic methods, ranging from the traditional techniques to the advanced molecular approaches, are explored, highlighting their strengths and limitations. The evolving landscape of treatment strategies, including antibiotic regimens and emerging therapeutic approaches, is thoroughly examined. Through a critical synthesis of the recent research findings, this article offers valuable insights into the contemporary knowledge of Helicobacter pylori infection, guiding both clinicians and researchers toward effective management and future directions in combating this global health challenge.

Helicobacter pylori (H. pylori) is one of the most prevalent human pathogens and the leading cause of chronic infection in almost half of the population in the world (~59%). The bacterium is a major leading cause of chronic gastritis, gastric and duodenal ulcers, and two type of malignancies, gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. Despite the immune responses mounted by the host, the bacteria are not cleared from the body resulting in a chronic infection accompanied by a chronic inflammation. Herein, a review of the literature discussing H. pylori antigens modulating the immune responses is presented. The mechanisms that are involved in the modulation of innate immune response, include modulation of recognition by pattern recognition receptors (PRRs) such as modulation of recognition by toll like receptors (TLR)4 and TLR5, modulation of phagocytic function, and modulation of phagocytic killing mediated by reactive oxygen species (ROS) and nitric oxide (NO). On the other hands, H. pylori modulates acquired immune response by the induction of tolerogenic dendritic cells (DCs), modulation of apoptosis, induction of regulatory T cells, modulation of T helper (Th)1 response, and modulation of Th17 response.

Listeria monocytogenes is motile at 22°C and non-motile at 37°C. In contrast, expression of L. monocytogenes virulence factors is low at 22°C and up-regulated at 37°C. Here, we studied a character of L. monocytogenes near surface swimming (NSS) motility and its effects on adhesion patterns and invasion into epithelial cells. L. monocytogenes and its saprophytic counterpart L. innocua both grown at 22°C showed similar NSS characteristics including individual velocities, trajectory lengths, residence times, and an asymmetric distribution of velocity directions. Similar NSS patterns correlated with similar adhesion patterns. Motile bacteria, including both pathogenic and saprophytic species, showed a preference for adhering to the periphery of epithelial HEp-2 cells. In contrast, non-motile bacteria were evenly distributed across the cell surface, including areas over the nucleus. However, the uneven distribution of motile bacteria did not enhance the invasion into HEp-2 cells unless virulence factor production was up-regulated by the transient shift of the culture to 37°C. Motile L. monocytogenes grown overnight at 22°C and then shifted to 37°C for 2 h expressed invasion factors at the same level and invaded human cells up to five times more efficiently comparatively with non-motile bacteria grown overnight at 37°C. Taken together, obtained results demonstrated that (i) NSS motility and correspondent peripheral location over the cell surface did not depend on L. monocytogenes virulence traits; (ii) motility improved L. monocytogenes invasion into human HEp-2 cells within a few hours after the transition from the ambient temperature to the human body temperature.

Helicobacter pylori is considered one of the most prevalent human pathogenic microbes globally. It is the main cause of a number of gastrointestinal ailments, including peptic and duodenal ulcers, and gastric tumors with high mortality rates. Thus, eradication of H. pylori is necessary to prevent gastric cancer. Still, the rise in antibiotic resistance is the most important challenge for eradication strategies. Better consideration of H. pylori virulence factors, pathogenesis, and resistance is required for better eradication rates and, thus, prevention of gastrointestinal malignancy. This article is aimed to show the role of virulence factors of H. pylori. Some are involved in its survival in the harsh environment of the human gastric lumen, and others are related to pathogenesis and the infection process. Furthermore, this work has highlighted the recent advancement in H. pylori treatment, as well as antibiotic resistance as a main challenge in H. pylori eradication. Also, we tried to provide an updated summary of the evolving H. pylori control strategies and the potential alternative drugs to fight this lethal resistant pathogen. Recent studies have focused on evaluating the efficacy of alternative regimens (such as sequential, hybrid, concomitant treatment, vonoprazan (VPZ)-based triple therapy, high-dose PPI-amoxicillin dual therapy, probiotics augmented triple therapy, or in combination with BQT) in the effective eradication of H. pylori. Thus, innovating new anti-H. pylori drugs and establishing H. pylori databanks are upcoming necessities in the near future.

The bacterial flagellum is a rotary motor organelle and important virulence factor that propels motile pathogenic bacteria, such as Salmonella enterica, through their surroundings. Bacteriophages, or phages, are viruses that solely infect bacteria. As such, phages have myriad applications in the healthcare field, including phage therapy against antibiotic-resistant bacterial pathogens. Bacteriophage χ (Chi) is a flagellum-dependent (flagellotropic) bacteriophage, which begins its infection cycle by attaching its long tail fiber to the S. enterica flagellar filament as its primary receptor. The interactions between phage and flagellum are poorly understood, as are the reasons that χ only kills certain Salmonella serotypes while others entirely evade phage infection. In this study, we used molecular cloning, targeted mutagenesis, heterologous flagellin expression, and phage-host interaction assays to determine which domains within the flagellar filament protein flagellin mediate this complex interaction. We identified the antigenic N- and C-terminal D2 domains as essential for phage χ binding, with the hypervariable central D3 domain playing a less crucial role. Here, we report that the primary structure of the Salmonella flagellin D2 domains is the major determinant of χ adhesion. The phage susceptibility of a strain is directly tied to these domains. We additionally uncovered important information about flagellar function. The central and most variable domain, D3, is not required for motility in S. Typhimurium 14028s, as it can be deleted or its sequence composition can be significantly altered with minimal impacts on motility. Further knowledge about the complex interactions between flagellotropic phage χ and its primary bacterial receptor may allow genetic engineering of its host range for use as targeted antimicrobial therapy against motile pathogens of the χ-host genera Salmonella, Escherichia, or Serratia.

Recently, numerous publications on Helicobacter pylori (H. pylori) have been published, but bibliometric analyses on this research field are scarce. To address this gap, we conducted a bibliometric analysis to provide a comprehensive overview and to explore the current research states and hotspots in this field.

Publications on H. pylori from 2002 to 2021 were retrieved from the Web of Science Core Collection database (WoSCC). Trends in publications and citations were analyzed using Excel 2021. VOSviewer and Citespace were used to perform bibliometrics analysis.

36,266 publications on H. pylori were retrieved from the WoSCC database. In general, we observed an increasing trend in the number of publications over the past 20 years. The United States was the most productive and influential country, with the largest proportion of both publications and total citations. Helicobacter, US Department of Veterans Affairs, and Graham, David were the most productive journals, institutions and authors, respectively. Further analysis the co-occurrence and burst detection of keywords revealed that the most common keywords were "Helicobacter pylori," "gastric cancer," and "gastritis," all keywords were divided into eight main clusters, and the most important current research hotspot was the relationship between H. pylori infection and the changes of gut microbiota.

The United States has been the most productive and influential country on H. pylori research, and H. pylori-related research remains an active research field. The relationship between H. pylori infection and the changes of gut microbiota is a research hotspot attracting significant attention.

Helicobacter pylori is a gastric pathogen that infects nearly half of the global population and is recognized as a group 1 carcinogen by the Word Health Organization. The global rise in antibiotic resistance has increased clinical challenges in treating H. pylori infections. Biofilm growth has been proposed to contribute to H. pylori's chronic colonization of the host stomach, treatment failures, and the eventual development of gastric diseases. Several components of H. pylori have been identified to promote biofilm growth, and several of these may also facilitate antibiotic tolerance, including the extracellular matrix, outer membrane proteins, shifted morphology, modulated metabolism, efflux pumps, and virulence factors. Recent developments in therapeutic approaches targeting H. pylori biofilm have shown that synthetic compounds, such as small molecule drugs and plant-derived compounds, are effective at eradicating H. pylori biofilms. These combined topics highlight the necessity for biofilm-based research in H. pylori, to improve current H. pylori-targeted therapeutic approaches and alleviate relative public health burden. In this review we discuss recent discoveries that have decoded the life cycle of H. pylori biofilms and current biofilm-targeted treatment strategies.

Patients suffering from chronic gastritis and developing gastric mucosa atrophy are at increased risk of the development of gastric cancer. The diagnosis of chronic atrophic gastritis (CAG) is a complex procedure involving a detailed history taking, a thorough physical examination and the use of laboratory and instrumental diagnostic methods among which the endoscopy of the upper digestive tract is the cornerstone because it allows the assessment of the topography of gastritis and identification of erosions and areas of intestinal metaplasia with the use of NBI endoscopy. However, the diagnosis of CAG requires morphological examination of the gastric mucosa. So, in addition to assessing macroscopic changes in the gastric mucosa, it is necessary to take biopsy specimens in accordance with the protocols for their morphological and immunohistochemical examination. In the absence of specific diagnostic stigmas of CAG, close cooperation between a clinician, endoscopist and pathologist is necessary. The article presents systematized data on the histopathological assessment of the gastric mucosa atrophy to predict the risk of gastric cancer.

The gut microbiota plays an important role in human health, as it can affect host immunity and susceptibility to infectious diseases. Invasive intestinal candidiasis is strongly associated with gut microbiota homeostasis. However, the nature of the interaction between Candida albicans and gut bacteria remains unclear.

This review aimed to determine the nature of interaction and the effects of gut bacteria on C. albicans so as to comprehend an approach to reducing intestinal invasive infection by C. albicans.

This review examined 11 common gut bacteria's interactions with C. albicans, including Escherichia coli, Pseudomonas aeruginosa, Acinetobacter baumannii, Enterococcus faecalis, Staphylococcus aureus, Salmonella spp., Helicobacter pylori, Lactobacillus spp., Bacteroides spp., Clostridium difficile, and Streptococcus spp.

Most of the studied bacteria demonstrated both synergistic and antagonistic effects with C. albicans, and just a few bacteria such as P. aeruginosa, Salmonella spp., and Lactobacillus spp. demonstrated only antagonism against C. albicans.

Based on the nature of interactions reported so far by the literature between gut bacteria and C. albicans, it is expected to provide new ideas for the prevention and treatment of invasive intestinal candidiasis.

Helicobacter pylori infection often occurs in early childhood, and can last a lifetime if not treated with medication. H. pylori infection can also cause a variety of stomach diseases, which can only be treated with a combination of antibiotics. Combinations of antibiotics can cure H. pylori infection, but it is easy to relapse and develop drug resistance. Therefore, a vaccine is a promising strategy for prevention and therapy for the infection of H. pylori. After decades of research and development, there has been no appearance of any H. pylori vaccine reaching the market, unfortunately. This review summarizes the aspects of candidate antigens, immunoadjuvants, and delivery systems in the long journey of H. pylori vaccine research, and also introduces some clinical trials that have displayed encouraging or depressing results. Possible reasons for the inability of an H. pylori vaccine to be available over the counter are cautiously discussed and some propositions for the future of H. pylori vaccines are outlined.

Outer membrane vesicles (OMVs) are lipid-membrane-bounded nanoparticles that are released from Gram-negative bacteria via vesiculation of the outer membrane. They have vital roles in different biological processes and recently, they have received increasing attention as possible candidates for a broad variety of biomedical applications. In particular, OMVs have several characteristics that enable them to be promising candidates for immune modulation against pathogens, such as their ability to induce the host immune responses given their resemblance to the parental bacterial cell. Helicobacter pylori (H. pylori) is a common Gram-negative bacterium that infects half of the world's population and causes several gastrointestinal diseases such as peptic ulcer, gastritis, gastric lymphoma, and gastric carcinoma. The current H. pylori treatment/prevention regimens are poorly effective and have limited success. This review explores the current status and future prospects of OMVs in biomedicine with a special focus on their use as a potential candidate in immune modulation against H. pylori and its associated diseases. The emerging strategies that can be used to design OMVs as viable immunogenic candidates are discussed.

Helicobacter pylori (H. pylori) has coevolved with its human host for more than 100 000 years. It can safely colonize around the epithelium of gastric glands via their specific microstructures and proteins. Unless patients receive eradication treatment, H. pylori infection is always lifelong. However, few studies have discussed the reasons. This review will focus on the adhesion of H. pylori from the oral cavity to gastric mucosa and summarize the possible binding and translocation characteristics. Adhesion is the first step for persistent colonization after the directional motility, and factors related to adhesion are necessary. Outer membrane proteins, such as the blood group antigen binding adhesin (BabA) and the sialic acid binding adhesin (SabA), play pivotal roles in binding to human mucins and cellular surfaces. And this may offer different perspectives on eradication.

Background Previous studies have shown an inverse relationship between ulcerative colitis (UC) and Helicobacter pylori infections (HPI). Though these two conditions have opposite geographic distributions, there may also be a physiological explanation for the decreased incidence of H. pylori infections in patients with UC. The purpose of this study is to analyze trends and complication rates of ulcerative colitis patients with and without HPI. Materials and methods The National Inpatient Sample (NIS) database was queried for patients with a primary diagnosis of UC, stratified by the presence of H. pylori infection. Patient demographics, length of stay, total hospital charges, and mortality were compared by H. pylori status. Additionally, complication rates were also compared between the two groups. Chi-squared and independent t-tests were used to compare outcomes and demographics, and multiple logistic regression was used to analyze primary and secondary outcomes. Results Patients with UC and HPI had a lower mortality rate (8.22 vs. 3.48, P<0.05, adjusted odds ratio [AOR] 0.33) and lower hospital charges ($65,652 vs. $47,557, p<0.05, AOR 1) with similar length of stay. Patients with UC and HPI also had lower rates of intestinal perforation (2.16% vs. 1.12%, p=0.05, AOR 0.408) and intrabdominal abscess formation (0.89% vs. 0.12%, AOR 0.165, p=0.072), though this difference was not significant. From 2001 to 2013, the incidence of UC has increased while the incidence of HPI has decreased. Conclusions The lower hospital charges and mortality rate as well as decreased rates of intestinal perforation and abscess formation suggest that there may be a physiologic role that HPI plays in modulating UC. Further studies into the interaction of these two conditions would be beneficial in clarifying their relationship and may help guide treatment of UC.

The flagellum is an important organelle for the survival of bacteria and consists of a basal body, hook, and filament. The FlgE protein is the subunit of the hook that connects the basal body and the filament and determines the motility of bacteria. Also, flgE gene plays an essential role in flagellar biosynthesis, swimming ability and biofilm formation. Although the intact flagella and the major component filament have been extensively studied, so far, little is known about the comprehensive understanding of flagellar hook and FlgE. Here in this review, we summarize the structures of flagellar hook and its subunit FlgE in various species and physiological functions of FlgE, including the hook assembly, the structural characteristics of flagellar hook, the mechanical properties of hook, and the similarities and differences between FlgE (hook) and FlgG (distal rod), with special attention on the interaction of FlgE with other molecules, the antigenicity and pro-inflammatory effect of FlgE, and cross-linking of FlgE in spirochetes. We hope our summary of this review could provide a better understanding of the FlgE protein and provide some useful information for developing new effective antibacterial drugs in the future work.

Helicobacter spp., including the well-known human gastric pathogen H. pylori, can cause gastric diseases in humans and other mammals. They are Gram-negative bacteria that colonize the gastric epithelium and use their multiple flagella to move across the protective gastric mucus layer. The flagella of different Helicobacter spp. vary in their location and number. This review focuses on the swimming characteristics of different species with different flagellar architectures and cell shapes. All Helicobacter spp. use a run-reverse-reorient mechanism to swim in aqueous solutions, as well as in gastric mucin. Comparisons of different strains and mutants of H. pylori varying in cell shape and the number of flagella show that their swimming speed increases with an increasing number of flagella and is somewhat enhanced with a helical cell body shape. The swimming mechanism of H. suis, which has bipolar flagella, is more complex than that of unipolar H. pylori. H. suis exhibits multiple modes of flagellar orientation while swimming. The pH-dependent viscosity and gelation of gastric mucin significantly impact the motility of Helicobacter spp. In the absence of urea, these bacteria do not swim in mucin gel at pH < 4, even though their flagellar bundle rotates.