Recent studies have found that in addition to directly impacting the gastric microbiome, Helicobacter pylori (H. pylori) infection may cause intestinal microbial dysbiosis. However, most existing studies on the influence of H. pylori infection on the intestinal microbiome used fecal specimens with inconsistent conclusions. Only one limited study on 8 H. pylori-infected patients has previously assessed the impact of H. pylori infection on the microbiome of the entire gastrointestinal tract, finding no significant effect on the bacterial composition of the lower gastrointestinal tract.

This single-center cross-sectional study collected mucosa of the esophagus, stomach, small intestine, and colon, as well as gastric juice and feces from 120 participants of the H. pylori-infected group (HIG) and 30 of the healthy control group (HCG). 16S rRNA sequencing was applied to analyze the bacterial composition and functional pathways, and metagenomics was adopted to assess the composition of viruses, eukaryotes, and archaea in the feces, as well as the antibiotic resistance gene (ARG) and virulence factors of bacteria (VF).

Compared with the HCG, the alpha and beta diversity of bacteria in the mucosa of the whole digestive tract and the gastric juice of the HIG showed significant changes, with increased microbial dysbiosis index and significantly different compositions at the phylum and genus levels. Functional pathway analysis revealed that the metabolic characteristics of the flora changed in the HIG, with site-specific differences. Fecal specimens demonstrated no significant differences in the above indicators between the two groups. In addition, feces-based metagenomic analysis revealed that only eukaryotes had higher diversity in the HIG, whereas viruses and archaea showed no significant changes; the Shannon index of ARG increased; and VF showed no significant change.

This study revealed that H. pylori infection significantly influenced the diversity, composition, and metabolic functional pathway of bacteria in different parts of the digestive tract and the gastric juice. Moreover, fecal microbial composition may not fully represent the mucosal microbial composition of the gastrointestinal tract.

Chinese Clinical Trial Registry: ChiCTR2300073419.

Gastric cancer (GC) is one of the most common malignancies worldwide, and Helicobacter pylori (HP) infection is a well-established risk factor for its development. Programmed death-ligand 1 (PD-L1) expression is a crucial biomarker for predicting the efficacy of immune checkpoint inhibitors in cancer treatment. While HP infection and PD-L1 expression in GC may be linked, the relationship between them remains unclear, in part because there have been conflicting results reported from various studies.

To perform a meta-analysis to assess the relationship between HP and PD-L1 expression in patients with GC.

A systematic literature review was conducted using PubMed, Embase, Cochrane Library, and Web of Science databases. Observational studies that examined the association between HP infection and PD-L1 expression in patients with GC were included. Odds ratios and 95% confidence intervals were calculated to estimate the association. Heterogeneity was assessed using Cochrane's Q test and I² statistic. A random-effects model was used due to significant heterogeneity across studies.

Fourteen studies involving a total of 3069 patients with GC were included. The pooled analysis showed a significant association between HP infection and increased PD-L1 expression in GC tissues (odd ratio = 1.69, 95% confidence interval: 1.24-2.29, P < 0.001, I 2 = 59%). Sensitivity analyses confirmed the robustness of these findings. Subgroup analyses did not show significant variation based on geographic region, sample size, or method of PD-L1 assessment. Publication bias was minimal, as shown by funnel plots and Egger's regression test.

HP infection is associated with increased PD-L1 expression in GC, suggesting that HP status may influence the response to programmed cell death protein 1/PD-L1 blockade therapy.

Helicobacter pylori (H. pylori) infection affects approximately 50% of the global population. The predominant route of H. pylori transmission is through the oral pathway, making the oral cavity highly significant in its infection. This review focuses on the relationship between H. pylori and oral diseases, the influence of H. pylori infection on the oral microbiota, and the potential mechanisms involving certain oral pathogens.

To identify relevant studies, we conducted searches in PubMed, Google Scholar using keywords such as "Helicobacter pylori," "oral diseases, " "oral microorganisms, " without any date restrictions. The retrieved publications were subject to a review.

H. pylori infection is positively correlated with the occurrence of various oral diseases, such as dental caries, periodontitis, and oral lichen planus. H. pylori may affect the oral microbiota through various mechanisms, and there exists an interactive relationship between H. pylori and oral bacteria, including Streptococcus, Porphyromonas gingivalis (P. gingivalis), and Candida albicans (C. albicans).

H. pylori infection has a close relationship with certain oral diseases. H. pylori modulates oral microflora diversity and structure, while eradication therapy and medications have varying impacts on oral microbiota.

Microorganisms contribute to the pathogenesis of obesity, while more studies focus on gut microbiome. However, the relationship between oral microbiota and obesity has yet to be elucidated. This study was designed to investigate the similarities and differences in the effects of a high-fat diet on salivary and gut microbiota through mouse experiments, exploring the hypothesis that oral microbial mechanisms may contribute to obesity.

An obese mouse model was established in male C57BL/6J mice by feeding a high-fat diet, confirmed by body weight records and blood glucose tests. This study evaluated the physiological effects of the high-fat diet on mice. 16S rRNA sequencing technology was used to analyze changes in salivary and gut microbiota, and gas chromatography-mass spectrometry was employed to evaluate 17 short-chain and medium-chain fatty acids quantitatively.

The microbiota distribution in salivary was different between the high-fat diet (HFD) and normal chow diet (NCD) groups. At the genus level of salivary microbiota, Streptococcus and Escherichia were highly abundant in the HFD group. Rodentibacter and Turicibacter were more abundant in the NCD group. Regarding the gut microbiome, the diversity changes of gut microbiota are more significant than those of salivary microbiota. The HFD group had a significantly higher abundance of Kineothrix, Cryptobacteroides, and a lower abundance of CAG-485. Nine genera had consistent alterations in salivary and gut microbiota, among which Akkermansia, Lactobacillus, and Intestinimonas were significantly correlated with physiological indicators, and Muribaculum was significantly correlated with increased decanoic acid levels in the HFD group. The dysregulated nine genera were associated with significant upregulation of certain metabolic pathways of the HFD group, including the pentose phosphate, bacterial invasion of epithelial cells, and steroid biosynthesis pathways.

There are differences and similarities in the effects of HFD on salivary and gut microbiota. Certain genera of the oral-gut axis altered consistently by HFD may affect obesity through mechanisms involving metabolic pathways and inflammation.

This study aims to investigate the prevalence and association between characteristics, dietary habits, and other factors associated to Helicobacter pylori (H. pylori) infection, as well as the resistance of H. pylori to antibiotics and risk factors in Quanzhou. A minimally invasive string test combined with qPCR was used to investigate the relationship between H. pylori infection and several factors that were evaluated using a survey. Logistic analyses were performed to estimate the risk factors for the prevalence and antibiotic resistance of H. pylori. The H. pylori prevalence amounted to 52.60%, the clarithromycin and levofloxacin resistance rate of H. pylori were 48.92% and 44.59%, respectively. Logistic analyses showed that takeaway food emerged as a protective factor for H. pylori infection, while the consumption of soy products reduced the risk of clarithromycin resistance. Furthermore, high sugar, spicy food, frequent tea drinking, and hyperlipidemia increased the risk of H. pylori infection. Finally, the frequency of oral hygiene had an impact on levofloxacin resistance. The prevalence and resistance rate of H. pylori was found to be high in Quanzhou. Our results also showed that diet, hygiene, and disease prevention awareness play an importance role in H. pylori prevention and treatment.

Gastric precancerous lesions are thought to be precursors in the occurrence and development of gastric cancer through Correa's cascade. Recent studies have investigated the association between the oral microbiome and gastric precancerous lesions. However, there has yet to be a comprehensive synthesis review of the existing literature on the relationship between oral microbiome and gastric precancerous lesions. A systematic review was conducted to characterize the literature on the association between oral microbiome and gastric precancerous lesions. The studies show that oral microbiome is dynamic in individuals with gastric precancerous lesions. Oral-derived microorganisms were colonized in the gastric precancerous lesions. Interactions between oral and gastric microbiomes affect the response of the host immunity. The abnormal proliferation of oral-associated microorganisms may be linked to the reduction of gastric acid. The present review supports the potential association between oral microbiome and gastric precancerous lesions. However, the interactions are complex and multifaceted, which require further investigation.

The oral-gut microbiota axis plays a crucial role in cardiometabolic health. This review explores the interactions between these microbiomes through enteric, hematogenous, and immune pathways, resulting in disruptions in microbial balance and metabolic processes. These disruptions contribute to systemic inflammation, metabolic disorders, and endothelial dysfunction, which are closely associated with cardiometabolic diseases. Understanding these interactions provides insights for innovative therapeutic strategies to prevent and manage cardiometabolic diseases.

Emerging evidence indicates that oral microbes are closely related to gastric microbes and gastric lesions, including gastric atrophy, intestinal metaplasia and gastric cancer (GC). Helicobacter pylori is a key pathogen involved in GC. However, the increasing prevalence of H. pylori-negative GC and gastric dysbiosis in GC patients emphasize the potential role of other microbial factors. In this review, we discussed the current evidence about the relationship between the oral-gastric microbial axis and oral and gastric health. Epidemiologic evidence indicates that poor oral hygiene is related to greater GC risk. Multiple oral-associated microbes are enriched in the stomach of GC patients. Once colonizing the stomach, oral-associated microbes Streptococcus anginosus and Prevotella melaninogenica, are involved in gastric inflammation or carcinogenesis. Microbial metabolites such as lactate, nitrite, and acetaldehyde promote malignant transformation. The stomach, as a checkpoint of microbial transmission in the digestive tract, is of great importance since the link between oral microbes and intestinal diseases has been emphasized. Still, new technologies and standardized metrics are necessary to identify potential pathogenetic microbes for GC and the core microbiota, interactions, richness, colonization, location and effect (CIRCLE). In the future, oral microbes could be candidates for noninvasive indicators to predict gastric diseases.

The effects of Helicobacter pylori (Hp)-related chronic gastritis on gastrointestinal microorganisms or brain neurotransmitters are not fully understood. Here, this study selected SPF C57BL/6 mice to set up a Hp-related chronic gastritis experiment group and a blank control group, and used omics to explore the specific effects of Hp-related chronic gastritis on gastrointestinal microorganisms and brain neurotransmitters in mice. The Tyramine (TyrA) content in the female experiment group's brain was considerably reduced compared to the female control group (p < 0.01), and TyrA was strongly correlated with 13 gastrointestinal microorganisms with significant differences, such as Acinetobacter_baumannii (p < 0.05). The His content in the male experiment group's brain was significantly higher than that in the male control group (p < 0.05), and His was strongly correlated with four gastrointestinal microorganisms with significant differences, such as Acinetobacter_baumannii (p < 0.05). The Levodopa (DOPA) content in the female control group's brain was significantly lower than that in the male control group (p < 0.05), and DOPA was strongly correlated with 19 gastrointestinal microorganisms with significant differences, such as Achromobacter_xylosoxidans (p < 0.05). The contents of L-Glutamine (Gln), L-Glutamine (GABA), Noradrenaline hydrochloride (NE), and Adrenaline hydrochloride (E) in the female experiment group's brain were significantly lower than those in the male experiment group (p < 0.05), and Gln, GABA, NE, and E were strongly correlated with 41, 28, 40, and 33 gastrointestinal microorganisms with significant differences (p < 0.05), respectively. These results indicate that Hp-related chronic gastritis could affect gastrointestinal microorganisms and brain neurotransmitters in mice with certain gender differences, and the changes in brain neurotransmitters might be related to the changes in gastrointestinal microorganisms.

Helicobacter pylori (H. pylori), the only bacterium classified as a type I (definite) carcinogen, is strongly associated with the development of gastric inflammation and adenocarcinoma. It infects the stomach of approximately half of the global population, equivalent to nearly 4.4 billion people. However, due to physiological barriers in the stomach, microbial barriers and increased antibiotic resistance, the therapeutic efficiency of standard antibiotic therapy is limited and cannot meet the clinical needs in some areas. Combining stimulus-responsive biomaterials with certain stimuli is an emerging antibacterial strategy. Stimulus-responsive biomaterials can respond to chemical, biological or physical cues in the environment with corresponding changes in their own properties and functions, highlighting a more intelligent, targeting and efficient aspect for H. pylori therapy.

This review describes the critical obstacles in the current treatment of H. pylori, summarizes the recent advances in stimulus-responsive biomaterials against H. pylori by elucidating their working mechanisms and antibacterial performances under different types of stimuli (pH, enzymes, light, magnetic and ultrasound irradiations), and attempts to analyze the future prospects of such smart biomaterial for H. pylori eradication. Key Scientific Concepts of Review: Any characteristic property or change in the biomilieu at the H. pylori infected site (endogenous stimuli) or specific iatrogenic conditions in vitro (exogenous stimuli) can act as cues to activate or potentiate the antibacterial activity of responsive biomaterials. The responsiveness of these materials to endogenous stimuli enhances antimicrobial targeting, and makes physiological barriers that would otherwise hinder conventional H. pylori therapies a key factor in facilitating antibacterial effects. The responsiveness to exogenous stimuli greatly prolongs the action time of antimicrobial materials and pinpoints the site of infection, thereby reducing toxic side effects. These findings pave the way for the development of more precise and effective anti-H. pylori treatment.

As a complicated and heterogeneous condition, breast cancer (BC) has posed a tremendous public health challenge across the world. Recent studies have uncovered the crucial effect of human microbiota on various perspectives of health and disease, which include cancer. The oral-gut microbiome axis, particularly, have been implicated in the occurrence and development of colorectal cancer through their intricate interactions with host immune system and modulation of systemic inflammation. However, the research concerning the impact of oral-gut microbiome axis on BC remains scarce. This study focused on comprehensively reviewing and summarizing the latest ideas about the potential bidirectional relation of the gut with oral microbiota in BC, emphasizing their potential impact on tumorigenesis, treatment response, and overall patient outcomes. This review can reveal the prospect of tumor microecology and propose a novel viewpoint that the oral-gut microbiome axis can be a breakthrough point in future BC studies.

Helicobacter pylori infections have been suggested to be associated with several extra gastric maladies, including hepatobiliary cancer (HBC). However, reports on the relationship between H. pylori infection and HBC showed variable and contrasting findings. This study aimed to address these contrasting findings and clarify the effect of H. pylori infections on HBC. Thus, we performed a systematic literature review of published related studies and a meta-analysis of eight eligible publications.

Related studies were searched in various database websites namely PubMed, ScienceDirect, Google Scholar, and Cochrane Library. Eligible studies were collated, and data were extracted. The odds ratio (OR) and 95% confidence interval (CI) were computed and interpreted using Review Manager 5.4.

Our overall analysis showed a significant association between H. pylori infection and HBC risk. Post-outlier analysis revealed homogeneous data (I2 = 0%, p = 0.82) and significant association (OR: 2.63, 95% CI: 1.62-4.28, P < 0.0001). Subgroup analysis based on the method of diagnosis (PCR OR: 2.46, 95% CI: 1.37-4.42, P = 0.003; ELISA OR: 2.40, 95% CI = 0.99 - 5.85, P = 0.05)  showed almost similar associations and odds ratios, but only the PCR group (I2 = 0%, P = 0.72) showed homogeneity. Subgroup analysis based on specimen types revealed consistent results for liver tissue (I2 = 0%, P = 0.82) and bile (I2= 0%, P = 0.76) samples, showing low heterogeneity. In contrast, serum samples (OR: 2.40, 95% CI = 0.99 - 5.85, P = 0.05) displayed a potential but statistically nonsignificant association, while bile samples demonstrated a significant association (OR: 3.65, 95% CI: 1.56-8.52, P = 0.003).

Overall, the present study suggests that H. pylori infection is associated with increased susceptibility to HBC development, with an increased effect found in bile and serum samples as specimens of choice for diagnosing H. pylori.

The bidirectional link of periodontitis (PD) and gastrointestinal tract (GIT) disorders has been investigated in previous epidemiological studies; however, the conclusions still remain controversial. The aim of this study was to comprehensively explore the bidirectional causal effect between PD and various GIT diseases.

Based on summary-level data of genome-wide association studies (GWASs), a two-sample bidirectional Mendelian randomization (MR) study was undertaken. Single-nucleotide polymorphisms (SNPs) associated with PD or GIT disorders (chronic gastritis [CG], gastric ulcer [GU], duodenal ulcer [DU], gastroesophageal reflux disease [GERD], irritable bowel syndrome [IBS], and diverticular disease of the intestine [DI]) in GWASs were applied as exposure. The primary method employed was the inverse-variance weighted (IVW) method, and several sensitivity analyses were performed to investigate potential pleiotropy.

With regard to the investigation of the causality between PD and GIT disorders, the IVW method revealed that there is a causal impact of PD on GU (odds ratio [OR] 1.088; 95% confidence interval [CI], 1.036-1.141; adjusted p = 0.004) and DI (OR 0.938; 95% CI, 0.911-0.965; adjusted p = 0.000). However, no significant genetic liability was observed for the causal effect of PD on CG, DU, GERD, and IBS. Furthermore, the primary analysis did not demonstrate a causal effect of GIT disorders on PD.

This MR study suggests that PD may be associated with an increased risk of GU and a reduced risk of DI, with possibly limited clinical relevance. Further studies are needed to support the conclusions of this MR study.

The oral cavity may play a role as a reservoir and in the transmission and colonization of Helicobacter pylori. The route of transmission for H. pylori is not fully understood. The prevalence of this pathogen varies globally, affecting half of the world's population, predominantly in developing countries. Here, we review the prevalence of H. pylori in the oral cavity, the characteristics that facilitate its colonization and dynamics in the oral microbiome, the heterogeneity and diversity of virulence of among strains, and noninvasive techniques for H. pylori detection in oral samples. The prevalence of H. pylori in the oral cavity varies greatly, being influenced by the characteristics of the population, regions where samples are collected in the oral cavity, and variations in detection methods. Although there is no direct association between the presence of H. pylori in oral samples and stomach infection, positive cases for gastric H. pylori frequently exhibit a higher prevalence of the bacterium in the oral cavity, suggesting that the stomach may not be the sole reservoir of H. pylori. In the oral cavity, H. pylori can cause microbiome imbalance and remodeling of the oral ecosystem. Detection of H. pylori in the oral cavity by a noninvasive method may provide a more accessible diagnostic tool as well as help prevent transmission and gastric re-colonization. Further research into this bacterium in the oral cavity will offer insights into the treatment of H. pylori infection, potentially developing new clinical approaches.

Helicobacter pylori infection is acquired in childhood via the oral cavity, although its relationship with the characteristics of the oral microbiome has not been elucidated. In this study, we performed comprehensive analysis of the oral microbiome in children and adults with or without H. pylori in the oral cavity.

Bacterial DNA was extracted from 41 adult and 21 child saliva specimens, and H. pylori was detected using PCR. 16S rRNA gene amplification was performed for next-generation sequencing. Bioinformatic analyses were conducted using Quantitative Insights into Microbial Ecology 2 (QIIME 2).

Faith's phylogenetic diversity analysis showed a significant difference between H. pylori-negative adult and child specimens in terms of α-diversity (p < 0.05), while no significant difference was observed between H. pylori-positive adult and child specimens. There was also a significant difference in β-diversity between H. pylori-positive and negative child specimens (p < 0.05). Taxonomic analysis at the genus level revealed that Porphyromonas was the only bacterium that was significantly more abundant in both H. pylori-positive adults and children than in corresponding negative specimens (p < 0.01 and p < 0.05, respectively).

These results suggest unique oral microbiome characteristics in children with H. pylori infection in the oral cavity.

More than half of the world's population are colonized with H. pylori; however, the prevalence varies geographically with the highest incidence in Africa. H. pylori is probably a commensal organism that has been associated with the development of gastritis, ulcers, and gastric cancer. H. pylori alone is most probably not enough for the development of gastric carcinoma, but evidence for its association with the disease is high and has, therefore, been classified by the International Agency for Research on Cancer as a Class 1 carcinogen. Bacteroidetes and Fusobacteria positively coexisted during H. pylori infection along the oral-gut axis. The eradication therapy required to treat H. pylori infection can also have detrimental consequences for the gut microbiota, leading to a decreased alpha diversity. Therefore, therapy regimens integrated with probiotics may abolish the negative effects of antibiotic therapy on the gut microbiota. These eradication therapies combined with probiotics have also higher rates of eradication, when compared to standard treatments, and are associated with reduced side effects, improving the patient's compliance. The eradication therapy not only affects gut microbiome but also affects the oral microbiome with robust predominance of harmful bacteria. However, there have been reports of a protective role of H. pylori in Barrett's esophagus, esophageal adenocarcinoma, eosinophilic esophagitis, IBD, asthma, and even multiple sclerosis. Therefore, eradication therapy should be carefully considered, and test to treat policy should be tailored to specific communities especially in highly endemic areas. Supplementation of probiotics, prebiotics, herbals, and microbial metabolites to reduce the negative effects of eradication therapy should be considered. After failure of many eradication attempts, the benefits of H. pylori eradication should be carefully balanced against the risk of adverse effects especially in the elderly, persons with frailty, and intolerance to antibiotics.

Helicobacter pylori (H. Pylori), is an established causative factor for the development of gastric cancer and the induction of persistent stomach infections that may lead to peptic ulcers. In recent decades, several endeavours have been undertaken to develop a vaccine for H. pylori, although none have advanced to the clinical phase. The development of a successful H. pylori vaccine is hindered by particular challenges, such as the absence of secure mucosal vaccines to enhance local immune responses, the absence of identified antigens that are effective in vaccinations, and the absence of recognized indicators of protection.

The DNA vaccine was chemically cloned, and the cloning was verified using PCR and restriction enzyme digestion. The efficacy of the vaccination was investigated. The immunogenicity and immune-protective efficacy of the vaccination were assessed in BALB/c mice. This study demonstrated that administering a preventive Alginate/pCI-neo-UreH Nanovaccine directly into the stomach effectively triggered a robust immune response to protect against H. pylori infection in mice.

The level of immune protection achieved with this nano vaccine was similar to that observed when using the widely accepted formalin-killed H. pylori Hel 305 as a positive control. The Alginate/pCI-neo-UreH Nanovaccine composition elicited significant mucosal and systemic antigen-specific antibody responses and strong intestinal and systemic Th1 responses. Moreover, the activation of IL-17R signaling is necessary for the defensive Th1 immune responses in the intestines triggered by Alginate/pCI-neo-UreH.

Alginate/pCI-neo-UreH is a potential Nanovaccine for use in an oral vaccine versus H. pylori infection, according to our findings.

This study established a high-throughput multiplex genetic detection assay (HMGA) for rapid identification, semi-quantification and virulence analysis of Helicobacter pylori directly from the clinical non-invasive oral samples.

The gastric mucosa and oral samples were collected from 242 patients in Shanghai from 2021 to 2022. All the samples were detected by routine clinical tests for H. pylori and Sanger sequenced for inconsistent results. A new multiplex PCR assay providing results within 4 hours was designed and optimized involving fluorescent dye-labeled specific primers targeted 16S rRNA gene, semi-quantitative gene ureC and 10 virulence genes of H. pylori. Semi-quantification was carried out by simulating the serial 10-fold dilutions of positive oral samples, and the H. pylori loads in different clinical samples were further compared. The mixed plasmids of virulence genes vacA s1, vacA m1 and vacA m2 were used to evaluate the performance on different genotypes. The consistency of 10 virulence genes in gastric mucosa, saliva, mouthwash and dental plaque of H. pylori-positive patients was compared.

The non-invasive HMGA was highly specific for detection of all 12 targets of H. pylori and human internal reference gene β-globin, and the sensitivity to all target genes could reach 10 copies/μL. Compared with routine clinical tests and sequencing, non-invasive HMGA has a high level (>0.98) of sensitivity, specificity, accuracy, PPV, NPV and kappa coefficient for direct detection of H. pylori in oral samples. Moreover, by detecting peak area levels of ureC, it was confirmed that the H. pylori loads in gastric mucosa were significantly higher than those of the three kinds of oral samples (p<0.05). We also found that 45.0% (91/202) of patients had different H. pylori virulence genes in different oral samples. The concordance of positive detection rates of each virulence gene between saliva and gastric mucosa was more than 78% (p<0.05).

The non-invasive HMGA proved to be a reliable method for the rapid H. pylori identification, semi-quantification and detection of 10 virulence genes directly in oral samples, providing a new idea for non-invasive detection of H. pylori.

The stomach was once considered a sterile organ until the discovery of Helicobacter pylori (HP). With the application of high-throughput sequencing technology and macrogenomics, researchers have identified fungi and fivemajor bacterial phyla within the stomachs of healthy individuals. These microbial communities exert regulatory influence over various physiological functions, including energy metabolism and immune responses. HP is a well-recognized risk factor for gastric cancer, significantly altering the stomach's native microecology. Currently, numerous studies are centered on the mechanisms by which HP contributes to gastric cancer development, primarily involving the CagA oncoprotein. However, aside from exogenous infections such as HP and EBV, certain endogenous dysbiosis can also lead to gastric cancer through multiple mechanisms. Additionally, gut microbiota and its metabolites significantly impact the development of gastric cancer. The role of microbial therapies, including diet, phages, probiotics and fecal microbiota transplantation, in treating gastric cancer should not be underestimated. This review aims to study the mechanisms involved in the roles of exogenous pathogen infection and endogenous microbiota dysbiosis in the development of gastric cancer. Also, we describe the application of microbiota therapy in the treatment and prognosis of gastric cancer.

Oral cavity is an essential reservoir for H. pylori. We aimed to investigate the antibacterial effects of dimethylaminododecyl methacrylate (DMADDM) against H. pylori. Modified giomers were prepared by introducing 0%, 1.25% and 2.5% DMADDM monomers. Broth microdilution assay, spot assay, Alamer Blue assay, PMA-qPCR, crystal violet staining, scanning electron microscopy observation and live/dead bacterial staining were performed to evaluate the antibacterial and antibiofilm effects of DMADDM and modified giomers in vitro. Urease assay, qPCR, hematoxylin-eosin staining and ELISA were performed to evaluate the inflammation levels and colonization of H. pylori in vivo. In vitro experiments indicated that the minimum inhibitory concentration and minimum bactericidal concentration of DMADDM were 6.25 μg/mL and 25 μg/mL, respectively. It inhibited H. pylori in a dose- and time-dependent manner, and significantly reduced the expression of cagA, vacA, flaA and ureB. DMADDM-modified giomers inhibited the formation of H. pylori biofilm and reduced live cells within it. In vivo experiments confirmed that the pretreatment with DMADDM-modified dental resin effectively reduced the gastric colonization of oral-derived H. pylori, suppressed systemic and local gastric inflammation. DMADDM monomers and DMADDM-modified giomers possessed excellent antibacterial and antibiofilm effects on H. pylori. Pretreatment with DMADDM-modified giomers significantly inhibited the gastric infection by H. pylori.

GIM is a persistent, premalignant lesion whereby gastric mucosa is replaced by metaplastic mucosa resembling intestinal tissue, arising in the setting of chronic inflammation, particularly in the context of Helicobacter pylori. While the overall rates of progression to gastric adenocarcinoma are low, estimated at from 0.25 to 2.5%, there are features that confer a much higher risk and warrant follow-up. In this review, we collate and summarise the current knowledge regarding the pathogenesis of GIM, and the clinical, endoscopic and histologic risk factors for cancer. We examine the current state-of-practice with regard to the diagnosis and management of GIM, which varies widely in the published guidelines and in practice. We consider the emerging evidence in population studies, artificial intelligence and molecular markers, which will guide future models of care. The ultimate goal is to increase the detection of early gastric dysplasia/neoplasia that can be cured while avoiding unnecessary surveillance in very low-risk individuals.

MiRNAs are short, non-coding RNA molecules, which are involved in the regulation of gene expression and which play an important role in various biological processes, including inflammation and cell cycle regulation. The possibility of detecting their extracellular expression, within body fluids, represented the main background for their potential use as non-invasive biomarkers of various diseases. Salivary miRNAs particularly gained interest recently due to the facile collection of stimulated/unstimulated saliva and their stability among healthy subjects. Furthermore, miRNAs seem to represent biomarker candidates of gastrointestinal disorders, with miRNA-based therapeutics showing great potential in those conditions. This review aimed to highlight available evidence on the role of salivary miRNAs in different gastrointestinal conditions. Most salivary-based miRNA studies available in the literature that focused on pathologies of the gastrointestinal tract have so far been conducted on pancreatic cancer patients and delivered reliable results. A few studies also showed the diagnostic utility of salivary miRNAs in conditions such as esophagitis, esophageal cancer, colorectal cancer, or inflammatory bowel disease. Moreover, several authors showed that salivary miRNAs may confidently be used as biomarkers of gastric cancer, but the use of salivary miRNA candidates in gastric inflammation and pre-malignant lesions, essential stages of Correa's cascade, is still put into question. On the other hand, besides miRNAs, other salivary omics have shown biomarker potential in gastro-intestinal conditions. The limited available data suggest that salivary miRNAs may represent reliable biomarker candidates for gastrointestinal conditions. However, their diagnostic potential requires validation through future research, performed on larger cohorts.

Helicobacter pylori (H. pylori) is significantly linked to various diseases that seriously impact human health, such as gastric ulcers, chronic gastritis and gastric adenocarcinoma.

The compositional shifts in bacterial communities of the orointestinal axis were surveyed pre/post-eradication of H. pylori. In total, 60 samples, including stool and salivary specimens, were collected from 15 H. pylori-positive individuals (HPP) before beginning and 2 months after receiving the eradication therapy. The V3-V4 regions of the 16S rRNA gene were sequenced using MiSeq.

Overall, oral microbiomes were collectively more diverse than the gut microbiomes (Kruskal-Wallis; p = 3.69 × 10^-5). Notably, the eradication of H. pylori was associated with a significant reduction in the bacterial diversity along the orointestinal axis (Wilcoxon rank sum test; p = 6.38 × 10^-3). Interestingly, the oral microbiome of HPP showed a positive correlation between Proteobacteria and Fusobacteria, in addition to a significant predominance of Streptococcus, in addition to Eubacterium_eligens, Haemophilus, Ruminococcaceae, Actinomyces and Staphylococcus. On the other hand, Fusobacterium, Veillonella, Catenibacterium, Neisseria and Prevotella were significantly enriched upon eradication of H. pylori. Generally, Bacteroidetes and Fusobacteria positively coexisted during H. pylori infection along the orointestinal axis (r = 0.67; p = 0.0006). The eradication of H. pylori was positively linked to two distinctive orotypes (O3 and O4). Orotype O4 was characterized by a robust abundance of Veillonella and Fusobacteria. The gut microbiomes during H. pylori infection showed a remarkable predominance of Clostridium_sensu_stricto_1 and Escherichia_Shigella. Likewise, Bifidobacterium and Faecalibacterium were significantly enriched upon eradication of H. pylori.

Finally, the impact of eradication therapy clearly existed on the representation of certain genera, especially in the oral microbiome, which requires particular concern in order to counteract and limit their subsequent threats.

Helicobacter pylori is a widespread helical Gram-negative bacterium, which causes a variety of stomach disorders, such as peptic ulcer, chronic atrophic gastritis, and gastric cancer. This microbe frequently colonizes the mucosal layer of the human stomach and survives in the inhospitable microenvironment, by adapting to this hostile milieu.

In this extensive review, we describe conventional antibiotic treatment regimens used against H. pylori including, empirical, tailored, and salvage therapies. Then, we present state-of-the-art information about reasons for treatment failure against H. pylori. Afterward, the latest advances in the use of probiotic bacteria against H. pylori infection are discussed. Finally, we propose a polymeric bio-platform to provide efficient delivery of probiotics for H. pylori infection.

For effective probiotic delivery systems, it is necessary to avoid the early release of probiotics at the acidic stomach pH, to protect them against enzymes and antimicrobials, and precisely target H. pylori bacteria which have colonized the antrum area of the stomach (basic pH).

Helicobacter pylori (H. pylori) is a Gram-negative anaerobic bacterium that colonizes the human stomach and is the leading cause of gastric diseases such as chronic gastritis and peptic ulcers, as well as the most definite and controllable risk factor for the development of gastric cancer. Currently, the regimen for H. pylori eradication has changed from triple to quadruple, the course of treatment has been extended, and the type and dose of antibiotics have been adjusted, with limited improvement in efficacy but gradually increasing side effects and repeated treatment failures in an increasing number of patients. In recent years, probiotics have become one of the most important tools for supporting intestinal health and immunity. Numerous in vitro studies, animal studies, and clinical observations have demonstrated that probiotics have the advantage of reducing side effects and increasing eradication rates in adjuvant anti-H. pylori therapy and are a valuable supplement to conventional therapy. However, many different types of probiotics are used as adjuncts against H. pylori, in various combinations, with different doses and timing, and the quality of clinical studies varies, making it difficult to standardize the results. In this paper, we focus on the risk, status, prevention, control, and treatment of H. pylori infection and review international consensus guidelines. We also summarize the available scientific evidence on using Limosilactobacillus reuteri (L. reuteri) as a critical probiotic for H. pylori treatment and discuss its clinical research and application from an evidence-based perspective.