Impact of Helicobacter pylori infection on fluid duodenal microbial community structure and microbial metabolic pathways

Background The bioactivities of commensal duodenal microbiota greatly influence the biofunction of hosts. We investigated the role of Helicobacter pylori infection in extra-gastroduodenal diseases by determining the impact of H. pylori infection on the duodenal microbiota. We sequenced 16 S rRNA genes in samples aspirated from the descending duodenum of 47 (male, 20; female, 27) individuals who were screened for gastric cancer. Samples were analysed using 16 S rRNA gene amplicon sequencing, and the LEFSe and Kyoto Encyclopaedia of Genes and Genomes methods were used to determine whether the duodenal microflora and microbial biofunctions were affected using H. pylori infection. Results Thirteen and 34 participants tested positive and negative for H. pylori, respectively. We identified 1,404 bacterial operational taxonomic units from 23 phyla and 253 genera. H. pylori infection changed the relative mean abundance of three phyla (Proteobacteria, Actinobacteria, and TM7) and ten genera (Neisseria, Rothia, TM7-3, Leptotrichia, Lachnospiraceae, Megasphaera, F16, Moryella, Filifactor, and Paludibacter). Microbiota features were significantly influenced in H. pylori-positive participants by 12 taxa mostly classified as Gammaproteobacteria. Microbial functional annotation revealed that H. pylori significantly affected 12 microbial metabolic pathways. Conclusions H. pylori disrupted normal bacterial communities in the duodenum and changed the biofunctions of commensal microbiota primarily by upregulating specific metabolic pathways. Such upregulation may be involved in the onset of diseases associated with H. pylori infection.

Análisis del agua de consumo humano abastecida por SEDAM huancayo para una propuesta de tratamiento en el control del Helicobacter pylori

La presencia del Helicobacter pylori en el agua contaminada es común, pero debido a que en Huancayo existe un buen número de personas con gastritis, úlcera gástrica, úlcera duodenal y cáncer al estómago, nos conduce a investigar la presencia de esta bacteria en el agua de consumo humano abastecida por la empresa SEDAM Huancayo. Se ha encontrado presencia del H. pylori en el agua de consumo humano de Huancayo convirtiéndose en un foco de infección y aparición de estas enfermedades en el habitante huancaíno. El presente es un estudio de análisis que se ha caracterizado por la toma de 50 muestras del agua para consumo humano abastecida por SEDAM Huancayo (de las 2 plantas de tratamiento y 08 pozos tubulares) los que han sido sometidos a pruebas de laboratorio. Se realizaron pruebas de cultivo e inmunología a fin de detectar el nivel de presencia del Helicobacter pylori en el agua. Se ha utilizado el método hipotético deductivo, por cuanto la deducción, tiene a su favor que sigue pasos sencillos, lógicos y obvios que permiten el descubrimiento de aquello que hemos pasado por alto. A través de la inducción, encontramos aspectos importantes a tener en cuenta para realizar una investigación como por ejemplo la cantidad de elementos del objeto de estudio. Entre los principales resultados tenemos que se ha encontrado la presencia del Helicobacter pylori en las 50 muestras de agua examinadas, tomadas por muestreo en la planta de tratamiento, pozos tubulares y domicilios. El tratamiento del agua de consumo humano que viene aplicando SEDAM Huancayo no está destinado al control del H. pylori. Sugerimos mejorar la cantidad y calidad del cloro que se diluye en el agua. Mejorando también en la forma de cloración del agua, para garantizar su pureza y hacerla apta para el consumo humano. La empresa SEDAM debe mejorar el laboratorio de análisis de agua a fin de poder realizar análisis de bacterias como el Helicobacter pylori, así como contratar mayor número de personal profesional especializado para realizar estas funciones. Coordinar acciones con la DIGESA a fin de poder mejorar los análisis del agua que llega a la población y de esta manera contribuir a la prevención de enfermedades gastrointestinales. Coordinar acciones a nivel nacional (SEDAPAL y otras empresas que suministran agua de consumo humano) y a nivel internacional (México, EE. UU., Europa, etc.).

Antagonistic Activities of Lactobacillus rhamnosus JB3 Against Helicobacter pylori Infection Through Lipid Raft Formation

Helicobacter pylori is a Gram-negative pathogen that can increase the risk of stomach cancer in infected patients. H. pylori exploits lipid rafts to infect host cells. Infection triggers clustering of Lewis x antigen (Lex) and integrins in lipid rafts to facilitate H. pylori adherence to the gastric epithelium. H. pylori infection can be treated with probiotics containing lactic acid bacteria that offer numerous benefits to the host while lacking the side effects associated with antibiotic therapy. Previously, we showed that the cell-free supernatant (CFS) derived from Lactobacillus rhamnosus JB3 (LR-JB3) at a multiplicity of infection (MOI) of 25 attenuated the pathogenicity of H. pylori. In this study, we established a mucin model to simulate the gastric environment and to further understand the influence of mucin on the pathogenesis of H. pylori. Porcine stomach mucin dramatically upregulated H. pylori virulence gene expression, including that of babA, sabA, fucT, vacA, hp0499, cagA, and cagL, as well as the adhesion and invasion ability of H. pylori and induced increased levels of IL-8 in infected-AGS cells. The CFS derived from LR-JB3 at a MOI of 25 reduced the expression of H. pylori sabA, fucT, and hp0499 in mucin, as well as that of the Lex antigen and the α5β1 integrin in AGS cells during co-cultivation. These inhibitory effects of LR-JB3 also suppressed lipid raft clustering and attenuated Lewis antigen-dependent adherence, type IV secretion system-mediated cell contact, and lipid raft-mediated entry of VacA to host cells. In conclusion, LR-JB3 could affect H. pylori infection through mediating lipid raft formation of the host cells. The currently unknown cues secreted from LR-JB3 are valuable not only for treating H. pylori infection, but also for treating diseases that are also mediated by lipid raft signaling, such as cancer and aging-associated and neurodegenerative conditions.

Prevalence of H. Pylori Infection in Non-Cirrhotic Patients with Chronic Delta Hepatitis

Objective: The relationship between Hepatitis Delta infection and Helicobacter infection in patients with non-cirrhotic hepatitis B infection was retrospectively investigated. Material and Methods: Stool samples of 117 patients included with Delta hepatitis infection in the study At total 36 of them were tested for H. Pylori infection. To detect H. Pylori, stool samples were tested using a commercial stool H. Pylori antigen assay. Results: Of these, 13 (19%) patients had H. Pylori seropositivity in the Hepatitis B infection group and 23 (48%) patients tested positive for H. Pylori infection in hepatitis delta infection group. There was a statistically significant difference between groups regarding H. Pylori seropositivity by the faecal test (p= 0.001). Conclusion: This study provides new knowledge on H. Pylori infection and reflects the need for evidence-based and comorbid dieases-oriented guidelines in the field of gastroenterology.

Helicobacter Pylori Urease: Potential Contributions to Alzheimer’s Disease

Alzheimer’s disease (AD) causes dementia and memory loss in the elderly. Deposits of beta-amyloid peptide and hyperphosphorylated tau protein are present in AD’s brain. A filtrate of Helicobacter pylori’s culture was previously found to induce hyperphosphorylation of tau in vivo, suggesting that bacterial exotoxins could permeate the blood brain barrier and directly induce tau’s phosphorylation. H. pylori, which infects ~60% of the world population and causes gastritis and gastric cancer, produces a pro-inflammatory urease (HPU). Here the neurotoxic potential of HPU was investigated in cultured cells and in rats. SH-SY5Y neuroblastoma cells exposed HPU (50-300 nM) produced reactive oxygen species (ROS) and had an increased [Ca2+]i. HPU-treated BV-2 microglial cells produced ROS, cytokines IL-1β and TNF-α, expressed Iba1 and showed reduced viability, consistent with a neurotoxic effect of HPU. Rats received daily i.p. HPU (5 µg) for 7 days. Hyperphosphorylation of tau at Thr205, Ser199 and Ser396 sites was seen in hippocampal homogenates of treated rats, with no alterations in total tau or GSK-3b levels. HPU was not detected in the brain homogenates. Behavioral tests were performed to assess cognitive impairments. Our findings support previous data suggesting an association between infection by H. pylori and tauopathies such as AD, possibly mediated by its urease.

Risk Factors For Recurrence of Peptic Ulcer Disease: A Retrospective Study In Tertiary Care Referral Center

Backgrounds: Peptic ulcer disease (PUD) is a common gastrointestinal tract disease characterized by mucosal damage secondary to pepsin and gastric acid secretion. The aim of this study was to evaluate the five-year recurrence rate for treated patients with PUD and risk factors contributing to PUD relapses.Methods: From 2016 through 2021, all patients with endoscopy-proved PUD were identified by reviewing medical records (Best-Care system). Possible risk factors including smoking, non-steroidal anti-inflammatory drugs (NSAIDs), aspirin, alcohol, caffeine, and steroid were analyzed by univariate analysis. Treatment outcomes, 5-year recurrence rate, and mortality rate were assessed.Results: Among 223 patients, there were 187 (83.8%), who diagnosed endoscopy-proved PUD and 36 (16.2%), who diagnosed clinical PUD. Among them, 126 (56.5%) patients were males and the mean age was 62±2 years. The five years recurrence rate of PUD was 30.9%. There was no significant difference in the recurrence rate between the duodenal ulcer (33.3%) and the gastric ulcer (28.8%). By univariate analysis, the use of steroid and NSAID and H. pylori infection were potential risk factors for PUD (P < 0.005). The common complication of PUD was gastrointestinal bleeding (34.1%). Patients who had a complicated PUD were associated with a higher rate of recurrence (45.9%) compared to the uncomplicated PUD (19.2%) (P > 0.05). Conclusion: Our findings demonstrated that the five years recurrence rate of PUD was 30.9%. The use of steroid and NSAID and H. pylori infection were risk factors for recurrence of PUD. PUD places a significant burden on health care systems. Therefore, a multicenter prospective study is needed for effective management to prevent recurrence and complications of PUD.

Analysis of Influencing Factors on the Occurrence and Development of Gastric Cancer in High-Incidence Areas of Digestive Tract Tumors Based on High Methylation of GPX3 Gene

Stomach cancer is the second largest cause of cancer-related mortality globally, and it continues to be a reason for worry today. Inhalation of the stomach cancer risk factor H. pylori produces large levels of reactive oxygen species (ROS). When combined with glutathione reductase, glutathione peroxidase 3 (GPX3) catalyzes the reduction of hydrogen peroxide and lipid peroxides. To get a better understanding of the GPX3 gene’s role in the illness, the researchers used quantitative real-time RT-PCR to examine the gene’s expression and regulation in gastric cancer cell lines, original gastric cancer samples, and 45 normal stomach mucosa adjacent to malignancies. According to the research, GPX3 expression was decreased or silenced in eight of nine cancer cell lines and 83 percent of gastric cancer samples (90/108) as compared to normal gastric tissues in the vicinity of the tumor ( P < 0.0001 ). It was found that 60 percent of stomach cancer samples exhibited DNA hypermethylation after analyzing the GPX3 promoter ( P = 0.007 ) (a methylation level of more than 10 percent, as measured by bisulfite pyrosequencing). In stomach tumors, we found a statistically significant reduction in the amount of GPX3 DNA copies ( P < 0.001 ). The gene expression of SNU1 and MKN28 cells was restored after treatment with 5-Aza-2′ Deoxycytidine to reduce GPX3 promoter methylation. Genetic and epigenetic alterations lead GPX3 to be dysfunctional in gastric cancer. This indicates that the systems that regulate ROS have been disrupted, and GPX3 may be implicated in the development of gastric cancer, as shown by our results when evaluated alone and in combination.

Efficacy of Helicobacter pylori eradication therapy for functional dyspepsia: updated systematic review and meta-analysis

ObjectiveFunctional dyspepsia (FD) is a chronic disorder that is difficult to treat. Helicobacter pylori may contribute to its pathophysiology. A Cochrane review from 2006 suggested that eradication therapy was beneficial, but there have been numerous randomised controlled trials (RCTs) published since. We evaluated impact of eradication therapy on both cure and improvement of FD, as well as whether any benefit was likely to arise from eradication of H. pylori.DesignWe searched the medical literature through October 2021 to identify RCTs examining efficacy of eradication therapy in H. pylori-positive adults with FD. The control arm received antisecretory therapy or prokinetics, with or without placebo antibiotics, or placebo alone. Follow-up was for ≥3 months. We pooled dichotomous data to obtain a relative risk (RR) of symptoms not being cured or symptoms not improving with a 95% CI. We estimated the number needed to treat (NNT).ResultsTwenty-nine RCTs recruited 6781 H. pylori-positive patients with FD. Eradication therapy was superior to control for symptom cure (RR of symptoms not being cured=0.91; 95% CI 0.88 to 0.94, NNT=14; 95% CI 11 to 21) and improvement (RR of symptoms not improving=0.84; 95% CI 0.78 to 0.91, NNT=9; 95% CI 7 to 17). There was no significant correlation between eradication rate and RR of FD improving or being cured (Pearson correlation coefficient=−0.23, p=0.907), but the effect was larger in patients with successful eradication of H. pylori than with unsuccessful eradication (RR=0.65; 95% CI 0.52 to 0.82, NNT=4.5, 95% CI 3 to 9). Adverse events (RR=2.19; 95% 1.10 to 4.37) and adverse events leading to withdrawal (RR=2.60; 95% CI 1.47 to 4.58) were more common with eradication therapy.ConclusionThere is high quality evidence to suggest that H. pylori eradication therapy leads to both cure and improvement in FD symptoms, although the benefit is modest.

Helicobacter pylori Prevalence and Risk Factors in Three Rural Indigenous Communities of Northern Arizona

Helicobacter pylori (H. pylori) is one of the most common bacterial stomach infections and is implicated in a majority of non-cardia gastric cancer. While gastric cancer has decreased in the United States (US), the incidence in the Navajo Nation is nearly four times higher than surrounding Non-Hispanic White populations. Little is known about H. pylori prevalence in this population or other Indigenous communities in the lower 48 states. In this cross-sectional study, 101 adults representing 73 households from three Navajo Nation chapter communities completed surveys and a urea breath test for active H. pylori. Accounting for intrahousehold correlation, H. pylori prevalence was 56.4% (95% CI, 45.4–66.8) and 72% of households had at least one infected person. The odds of having an active infection in households using unregulated water were 8.85 (95% CI, 1.50–53.38) that of the use of regulated water, and males had 3.26 (95% CI, 1.05–10.07) higher odds than female. The prevalence of H. pylori in Navajo is similar to that seen in Alaska Natives. Further investigation into factors associated with prevention of infection is needed as well as understanding barriers to screening and treatment.