Acid Acclimation byHelicobacter pylori

Physiology ◽  
2005 ◽  
Vol 20 (6) ◽  
pp. 429-438 ◽  
Author(s):  
George Sachs ◽  
David L. Weeks ◽  
Yi Wen ◽  
Elizabeth A. Marcus ◽  
David R. Scott ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Carbonic Anhydrase ◽  
Human Stomach ◽  
Peptic Ulcers ◽  
Acidic Media ◽  
Gram Negative ◽  
Urea Channel ◽  
Acid Acclimation ◽  
Unique Ability

Helicobacter pylori is a Gram-negative neutralophile associated with peptic ulcers and gastric cancer. It has a unique ability to colonize the human stomach by acid acclimation. It uses the pH-gated urea channel, UreI, to enhance urea access to intrabacterial urease and a membrane-anchored periplasmic carbonic anhydrase to regulate periplasmic pH to ~6.1 in acidic media, whereas other neutralophiles cannot regulate periplasmic pH and thus only transit the stomach.

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 The Periplasmic α-Carbonic Anhydrase Activity of Helicobacter pylori Is Essential for Acid Acclimation

2005 ◽  
Vol 187 (2) ◽  
pp. 729-738 ◽  
Author(s):  
Elizabeth A. Marcus ◽  
Amiel P. Moshfegh ◽  
George Sachs ◽  
David R. Scott
Keyword(s):  
Helicobacter Pylori ◽  
Membrane Potential ◽  
Carbonic Anhydrase ◽  
Membrane Integrity ◽  
Carbonic Anhydrase Activity ◽  
Knockout Mutant ◽  
Inner Membrane ◽  
Acid Acclimation

ABSTRACT The role of the periplasmic α-carbonic anhydrase (α-CA) (HP1186) in acid acclimation of Helicobacter pylori was investigated. Urease and urea influx through UreI have been shown to be essential for gastric colonization and for acid survival in vitro. Intrabacterial urease generation of NH3 has a major role in regulation of periplasmic pH and inner membrane potential under acidic conditions, allowing adequate bioenergetics for survival and growth. Since α-CA catalyzes the conversion of CO2 to HCO3 −, the role of CO2 in periplasmic buffering was studied using an α-CA deletion mutant and the CA inhibitor acetazolamide. Western analysis confirmed that α-CA was bound to the inner membrane. Immunoblots and PCR confirmed the absence of the enzyme and the gene in the α-CA knockout. In the mutant or in the presence of acetazolamide, there was an ∼3 log10 decrease in acid survival. In acid, absence of α-CA activity decreased membrane integrity, as observed using membrane-permeant and -impermeant fluorescent DNA dyes. The increase in membrane potential and cytoplasmic buffering following urea addition to wild-type organisms in acid was absent in the α-CA knockout mutant and in the presence of acetazolamide, although UreI and urease remained fully functional. At low pH, the elevation of cytoplasmic and periplasmic pH with urea was abolished in the absence of α-CA activity. Hence, buffering of the periplasm to a pH consistent with viability depends not only on NH3 efflux from the cytoplasm but also on the conversion of CO2, produced by urease, to HCO3 − by the periplasmic α-CA.

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 Clinical and Endoscopic Features in Helicobacter Pylori Infection: Literature Review

2021 ◽  
Vol 22 (1) ◽  
pp. 66-72
Author(s):  
Ghina Tsuraya Salsabila Budiman ◽  
Muhammad Begawan Bestari ◽  
Sri Suryanti
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Functional Dyspepsia ◽  
Epigastric Pain ◽  
False Negative ◽  
Clinical Manifestations ◽  
Helicobacter Pylori Infection ◽  
Gastric Ulcers ◽  
Common Symptom ◽  
Peptic Ulcers

Helicobacter pylori is a common infection worldwide and can cause functional dyspepsia, gastritis, and peptic ulcers, leading to gastric cancer. The very diverse clinical outcomes and symptoms of this infection are difficult to distinguish from one another. Endoscopy is one of the methods used to detect Helicobacter pylori infection. Still, it has various endoscopic features, has the possibility of false-negative results, and requires skill to get the maximum results.This study found that infection can cause various clinical manifestations due to different virulence factors of Helicobacter pylori bacteria. In functional dyspepsia, the patient's most common symptoms are epigastric pain, nausea, and vomiting. In gastritis, Helicobacter pylori infection often causes chronic gastritis with topographic features of pangastritis, and endoscopic features that are usually found are redness, swelling, and regular arrangement of collecting venules (RAC). The most common symptom in peptic ulcers is pain that occurs after eating or at night, and this infection can cause duodenal and gastric ulcers. Currently, the relationship between Helicobacter pylori infection and gastroesophageal reflux disease (GERD) is controversial. In gastric cancer, the most common symptoms are weight loss and repeated vomiting. This infection is more likely to causes intestinal-type gastric cancer.

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.

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.

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.

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