scholarly journals Plant-Based Polyphenols: Anti-Helicobacter pylori Effect and Improvement of Gut Microbiota

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 109
Author(s):  
María Guerra-Valle ◽  
Patricio Orellana-Palma ◽  
Guillermo Petzold
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Antibiotic Resistance ◽  
Gut Microbiota ◽  
Bactericidal Effect ◽  
Potential Effect ◽  
Alternative Therapies ◽  
Peptic Ulcers ◽  
Health Promoting ◽  
H Pylori

Helicobacter pylori (H. pylori) infection affects more than half of the world’s population, and thus, about 10 to 20% of people with H. pylori suffer from peptic ulcers, which may ultimately lead to gastric cancer. The increase in antibiotic resistance and susceptibility has encouraged the search for new alternative therapies to eradicate this pathogen. Several plant species are essential sources of polyphenols, and these bioactive compounds have demonstrated health-promoting properties, such as the gut microbiota stimulation, inflammation reduction, and bactericidal effect. Therefore, this review aims to discuss the potential effect of plant-based polyphenols against H. pylori and their role in the gut microbiota improvement.

Increased Production of Matrix Metalloproteinases in Helicobacter pylori Infection that Stimulates Gastric Cancer Stem Cells

2020 ◽  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Helicobacter Pylori ◽  
Cancer Stem Cells ◽  
Histopathological Examination ◽  
Physiological Saline ◽  
Rrna Gene ◽  
Peptic Ulcers ◽  
Gastric Cancer Stem Cells ◽  
H Pylori

Background and aim: Helicobacter pylori (H. pylori) is an incriminated pathogen causing diseases in both animals and humans and considered a zoonotic pathogen. H. pylori infection is considered a cause of gastric cancer, which rests a significant health care challenge. This study analyzes the expression pattern of matrix metalloprotein 2 (MMP-2) in patients with Helicobacter pylori-associated gastritis and the effect of H. pylori on gastric cancer stem cells, as well as study the role of helicon bacteriosis in dog in transmission of H. pylori infection to human. Materials and methods: Fifty-five of each sample (gastric biopsy, blood and stool) were collected from patients suffering from dyspepsia, chronic vomiting and perforated peptic ulcers and also from apparent healthy dogs. The investigation detected H. pylori by serological and histopathological examination. Biopsies were stored in physiological saline for identification of H. pylori by conventional time PCR. MMP-2 and Gastric cancer stem cells were then identified by immunohistochemistry. Results: Serological identification for H. pylori Antigen and Antibodies revealed (63% human, 50% dogs) and (87% human, 90% dogs) respectively were positive. Genotyping of H. pylori based on 16S rRNA gene showed 54.5% of human and 35% of dogs were positive. Immunohistochemistry revealed strong expression of CD44 in H. pylori- associated gastric cancer cases, MMP-2 expression was observed in all neoplastic lesions associated with H. pylori infection. Conclusion: H. pylori infection affects gastric mucosa and induces changes in gastric stem cells altering their differentiation and increased expression of MMP’s and CD44with a resultant potentiation of oncogenic alteration. In addition the up-regulation of both markers could be an instrumental to interpret the origination of gastric cancer.

scholarly journals Cross-sectional study of human coding- and non-coding RNAs in progressive stages of Helicobacter pylori infection

2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Sergio Lario ◽  
María J. Ramírez-Lázaro ◽  
Aintzane González-Lahera ◽  
José L. Lavín ◽  
Maria Vila-Casadesús ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Expression Profiles ◽  
Gastric Carcinogenesis ◽  
Individual Response ◽  
Peptic Ulcers ◽  
Gastric Diseases ◽  
Sequence Of Events ◽  
Non Coding Rnas ◽  
H Pylori

Abstract Helicobacter pylori infects 4.4 billion individuals worldwide and is considered the most important etiologic agent for peptic ulcers and gastric cancer. Individual response to H. pylori infection is complex and depends on complex interactions between host and environmental factors. The pathway towards gastric cancer is a sequence of events known as Correa’s model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic-active gastritis, atrophy, metaplasia and gastric adenocarcinoma. This study examines gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profiles of coding- and non-coding RNAs that may have a role in Correa’s model of gastric carcinogenesis. We screened for differentially expressed genes in gastric biopsies by employing RNAseq, microarrays and qRT-PCR. Here we provide a detailed description of the experiments, methods and results generated. The datasets may help other scientists and clinicians to find new clues to the pathogenesis of H. pylori and the mechanisms of progression of the infection to more severe gastric diseases. Data is available via ArrayExpress.

scholarly journals Relationship between Helicobacter pylori iceA, cagA, and vacA Status and Clinical Outcome: Studies in Four Different Countries

1999 ◽  
Vol 37 (7) ◽  
pp. 2274-2279 ◽  
Author(s):  
Yoshio Yamaoka ◽  
Tadashi Kodama ◽  
Oscar Gutierrez ◽  
Jong G. Kim ◽  
Kei Kashima ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Clinical Outcome ◽  
Clinical Presentation ◽  
The United States ◽  
Peptic Ulcers ◽  
Predominant Genotype ◽  
Clinical Presentations ◽  
Geographic Differences ◽  
H Pylori

There is continuing interest in identifying Helicobacter pylori virulence factors that might predict the risk for symptomatic clinical outcomes. It has been proposed thaticeA and cagA genes are such markers and can identify patients with peptic ulcers. We compared H. pylori isolates from four countries, looking at thecagA and vacA genotypes, iceAalleles, and presentation of the infection. We used PCR to examineiceA, vacA, and cagA status of 424H. pylori isolates obtained from patients with different clinical presentations (peptic ulcer, gastric cancer, and atrophic gastritis). The H. pylori isolates examined included 107 strains from Bogota, Colombia, 70 from Houston, Tex., 135 from Seoul, Korea, and 112 from Kyoto, Japan. The predominant genotype differed among countries: the cagA-positive iceA1 vacA s1c-m1 genotype was predominant in Japan and Korea, thecagA-positive iceA2 vacA s1b-m1 genotype was predominant in the United States, and the cagA-positiveiceA2 vacA s1a-m1 genotype was predominant in Colombia. There was no association between the iceA,vacA, or cagA status and clinical outcome in patients in the countries studied. iceA status shows considerable geographic differences, and neither iceA nor combinations of iceA, vacA, andcagA were helpful in predicting the clinical presentation of an H. pylori infection.

scholarly journals Helicobacter pylori Eradication Therapy - Recent Trend in Research

2020 ◽  
Vol 20 (3) ◽  
pp. 210-217
Author(s):  
Heung Up Kim
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Antibiotic Resistance ◽  
Gastric Mucosa ◽  
Drug Exposure ◽  
Eradication Therapy ◽  
Dual Therapy ◽  
Resistance Rate ◽  
H Pylori ◽  
Selection Of

It is well known that <i>Helicobacter pylori (H. pylori)</i> can cause peptic ulcer, mucosa-associated lymphoid tissue lymphoma, atrophic gastritis, intestinal metaplasia, and ultimately, gastric cancer. Various studies have proven that <i>H. pylori</i>, which attaches to the gastric mucosa, is the cause of gastric cancer and can be eradicated using appropriate antibiotics. Since 2013, Japan has been carrying out national-led eradication treatment of <i>H. pylori</i> for the whole population. However, as drug exposure increases, the resistance rate to some antibiotics increases, and the pattern of antibiotic resistance varies from region to region. Therefore, the development of individualized antimicrobial therapies has become important since antibiotic resistance to <i>H. pylori</i> eradication is a problem worldwide. To help overcome this, remedies such as selection of antibiotics through susceptibility testing, selection of empirical treatment combinations appropriate for the region, dual therapy with high doses of amoxicillin, and the use of rifabutin or sitafloxacin with low antibiotic resistance have been studied. Potassium-competitive acid blocker has been reported to be more potent in inhibiting acid secretion than proton pump inhibitor, and its role in <i>H. pylori</i> eradication is expected. Drug formulations and regimens that are easy to take are being developed to increase compliance. New treatments such as spraying antibiotics directly to the gastric mucosa are being developed and studied.

scholarly journals Proinflammatory Activity of a Cecropin-Like Antibacterial Peptide from Helicobacter pylori

2001 ◽  
Vol 45 (6) ◽  
pp. 1700-1704 ◽  
Author(s):  
Johan Bylund ◽  
Thierry Christophe ◽  
Francois Boulay ◽  
Thomas Nyström ◽  
Anna Karlsson ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Antibacterial Properties ◽  
Bacterial Pathogen ◽  
Inflammatory Cells ◽  
Bactericidal Effect ◽  
Antibacterial Peptide ◽  
Human Neutrophils ◽  
Human Gastric Mucosa ◽  
Peptic Ulcers ◽  
H Pylori

ABSTRACT Helicobacter pylori, the bacterial pathogen associated with gastritis and peptic ulcers, is highly successful in establishing infection in the human gastric mucosa, a process typically associated with massive infiltration of inflammatory cells. Colonization of the mucosa is suggested to be facilitated by H. pylori-produced cecropin-like peptides with antibacterial properties, giving the microbe a competitive advantage over other bacteria. We show that a cecropin-like antibacterial peptide from H. pylori, Hp(2-20), not only has a potent bactericidal effect but also induces proinflammatory activities in human neutrophils, e.g., upregulation of integrins (Mac-1), induction of chemotaxis, and activation of the oxygen radical producing NADPH-oxidase. Furthermore, we show that these effects are mediated through binding of Hp(2-20) to the promiscuous, G-protein-linked lipoxin A4 receptor–formyl peptide-like receptor 1.

scholarly journals Inhibition of Helicobacter pylori and Gastric Cancer Cells by Lipid Aldehydes from Viburnum opulus (Adoxaceae)

2007 ◽  
Vol 2 (10) ◽  
pp. 1934578X0700201
Author(s):  
Maria Teresa Laux ◽  
Manuel Aregullin ◽  
Eloy Rodriguez
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Peptic Ulcers ◽  
Viburnum Opulus ◽  
Gastric Cancer Cells ◽  
H Pylori ◽  
Lipid Aldehydes

A unique group of bioactive, naturally occurring lipid aldehydes were isolated from the fruits of Viburnum opulus, (family Adoxaceae). The natural occurrences of these fatty acid derived aldehydes are reported here for the first time. Helicobacter pylori is a prevalent gastroduodenal pathogen, a causal agent of chronic gastritis and peptic ulcers and an important co-factor in gastric cancer development. We investigated the chemistry and bioactivity of these active constituents by evaluating their ability to inhibit the growth of H. pylori and to induce apoptosis in a gastric cancer cell line (CRL-5971) in vitro.

scholarly journals Galectin-2 Has Bactericidal Effects against Helicobacter pylori in a β-galactoside-Dependent Manner

2020 ◽  
Vol 21 (8) ◽  
pp. 2697 ◽  
Author(s):  
Takaharu Sasaki ◽  
Rei Saito ◽  
Midori Oyama ◽  
Tomoharu Takeuchi ◽  
Toru Tanaka ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Bactericidal Effect ◽  
Dependent Manner ◽  
Peptic Ulcers ◽  
Gastric Tissue ◽  
Gastric Mucus ◽  
Biological Phenomena ◽  
Bactericidal Effects ◽  
H Pylori

Helicobacter pylori is associated with the onset of gastritis, peptic ulcers, and gastric cancer. Galectins are a family of β-galactoside-binding proteins involved in diverse biological phenomena. Galectin-2 (Gal-2), a member of the galectin family, is predominantly expressed in the gastrointestinal tract. Although some galectin family proteins are involved in immunoreaction, the role of Gal-2 against H. pylori infection remains unclear. In this study, the effects of Gal-2 on H. pylori morphology and survival were examined. Gal-2 induced H. pylori aggregation depending on β-galactoside and demonstrated a bactericidal effect. Immunohistochemical staining of the gastric tissue indicated that Gal-2 existed in the gastric mucus, as well as mucosa. These results suggested that Gal-2 plays a role in innate immunity against H. pylori infection in gastric mucus.

Effective Reduction of Gastric Cancer Risk With Regular Use of Nonsteroidal Anti-Inflammatory Drugs in Helicobacter Pylori–Infected Patients

2010 ◽  
Vol 28 (18) ◽  
pp. 2952-2957 ◽  
Author(s):  
Chun-Ying Wu ◽  
Ming-Shiang Wu ◽  
Ken N. Kuo ◽  
Chang-Bi Wang ◽  
Yi-Ju Chen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Protective Factor ◽  
Nsaid User ◽  
Gastric Ulcers ◽  
Number Needed To Treat ◽  
Peptic Ulcers ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
H Pylori

Purpose Nonsteroidal anti-inflammatory drugs (NSAIDs) play protective roles in gastric carcinogenesis. However, the interaction between NSAIDs and Helicobacter pylori (H pylori) infection and the number needed to treat to prevent gastric cancer remains unclear. Patients and Methods We conducted a nationwide retrospective cohort study based on data from the Taiwan National Health Insurance Database. Hospitalized patients with a primary diagnosis of peptic ulcer disease were selected. Overall, 52,161 patients were divided into non-NSAID user and regular NSAID user cohorts. Standardized incidence ratios (SIRs), cumulative incidences, and hazard ratios (HRs) were calculated. Results Patients with peptic ulcers who never used NSAIDs had higher risk of gastric cancer compared with the general population (SIR, 2.11; 95% CI, 2.07 to 2.15), but regular NSAID use conferred lower risk (SIR, 0.79; 95% CI, 0.77 to 0.81). The protective role of NSAID use was observed in patients with gastric ulcer, but not in patients with non–H pylori-associated duodenal ulcer. On multivariate analysis, regular NSAID use was an independent protective factor for gastric cancer development (HR, 0.79 for each incremental year; P < .001), especially in H pylori-associated patients (HR, 0.52 for each incremental year; P < .001). Among patients with H pylori-infected gastric ulcers, the NNT to prevent a gastric cancer was 50. Conclusion Regular NSAID use may be a feasible way to prevent gastric cancer, at least in patients with gastric ulcers, and especially in H pylori-infected subjects.

scholarly journals Gut Microbiota: The Missing Link Between Helicobacter pylori Infection and Metabolic Disorders?

2021 ◽  
Vol 12 ◽  
Author(s):  
Gracia M. Martin-Nuñez ◽  
Isabel Cornejo-Pareja ◽  
Mercedes Clemente-Postigo ◽  
Francisco J. Tinahones
Keyword(s):  
Helicobacter Pylori ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Eradication Therapy ◽  
Future Research ◽  
Diabetic Patients ◽  
Peptic Ulcers ◽  
Hormonal Modulation ◽  
H Pylori ◽  
The Impact

Helicobacter pylori (H. pylori) is a gram-negative bacterium that infects approximately 4.4 billion individuals worldwide. Although the majority of infected individuals remain asymptomatic, this bacterium colonizes the gastric mucosa causing the development of various clinical conditions as peptic ulcers, chronic gastritis and gastric adenocarcinomas and mucosa-associated lymphoid tissue lymphomas, but complications are not limited to gastric ones. Extradigestive pathologies, including metabolic disturbances such as diabetes, obesity and nonalcoholic fatty liver disease, have also been associated with H. pylori infection. However, the underlying mechanisms connecting H. pylori with extragastric metabolic diseases needs to be clarified. Notably, the latest studies on the topic have confirmed that H. pylori infection modulates gut microbiota in humans. Damage in the gut bacterial community (dysbiosis) has been widely related to metabolic dysregulation by affecting adiposity, host energy balance, carbohydrate metabolism, and hormonal modulation, among others. Taking into account that Type 2 diabetic patients are more prone to be H. pylori positive, gut microbiota emerges as putative key factor responsible for this interaction. In this regard, the therapy of choice for H. pylori eradication, based on proton pump inhibitor combined with two or more antibiotics, also alters gut microbiota composition, but consequences on metabolic health of the patients has been scarcely explored. Recent studies from our group showed that, despite decreasing gut bacterial diversity, conventional H. pylori eradication therapy is related to positive changes in glucose and lipid profiles. The mechanistic insights explaining these effects should also be addressed in future research. This review will deal with the role of gut microbiota as the linking factor between H. pylori infection and metabolic diseases, and discussed the impact that gut bacterial modulation by H. pylori eradication treatment can also have in host’s metabolism. For this purpose, new evidence from the latest human studies published in more recent years will be analyzed.

scholarly journals Diversity of Helicobacter pylori vacA andcagA Genes and Relationship to VacA and CagA Protein Expression, Cytotoxin Production, and Associated Diseases

1998 ◽  
Vol 36 (4) ◽  
pp. 944-948 ◽  
Author(s):  
Jochen Rudi ◽  
Christof Kolb ◽  
Matthias Maiwald ◽  
Dirk Kuck ◽  
Andreas Sieg ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Signal Sequence ◽  
Peptic Ulcers ◽  
Virulence Determinants ◽  
Middle Region ◽  
Vacuolating Cytotoxin ◽  
Ulcer Disease ◽  
H Pylori

The vacuolating cytotoxin and the cytotoxin-associated protein, encoded by vacA and cagA, respectively, are important virulence determinants of Helicobacter pylori. Sixty-five H. pylori strains were isolated from dyspeptic patients (19 with peptic ulcer disease, 43 with chronic gastritis, and 3 with gastric cancer) and studied for differences in thevacA and cagA genes and their relationship to VacA and CagA expression, cytotoxin activity, and the clinical outcome of infection. By PCR, fifty-four (83.1%) of 65 strains had thevacA signal sequence genotype s1 and only 10 (15.4%) had the type s2. After primer modification, the vacAmiddle-region types m1 and m2 were detected in 24 (36.9%) and 41 (63.1%) strains, respectively. The combinations s1-m2 (31 [47.7%]) and s1-m1 (23 [35.4%]) occurred more frequently than s2-m2 (10 [15.4%]) (P = 0.01). No strain with the combination s2-m1 was found. All 19 patients with peptic ulcers harbored type s1 strains, in contrast to 32 (74.4%) of 43 patients with gastritis (P = 0.02). The vacA genotype s1 was associated with the presence of cagA (P < 0.0001), VacA expression (P < 0.0001), and cytotoxin activity (P = 0.003). The cagA gene was detectable in 48 (73.8%) of 65 isolates and present in 16 (84.2%) of 19 ulcer patients and 29 (67.4%) of 43 patients with gastritis (P = 0.17). The vacA genotypes of GermanH. pylori isolates are identical to those previously reported. H. pylori strains of vacA type s1 are associated with the occurrence of peptic ulceration and the presence ofcagA, cytotoxin activity, and VacA expression.

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