scholarly journals Toward a Better Understanding of the Role ofHelicobacter pyloriInfection as a Cause of Dyspepsia

2004 ◽  
Vol 18 (2) ◽  
pp. 136-137
Author(s):  
Frank YH Lin ◽  
Philip M Sherman
Keyword(s):  
Helicobacter Pylori ◽  
Murine Model ◽  
Chronic Infection ◽  
Acute Infection ◽  
Histological Evaluation ◽  
Polymorphonuclear Cell ◽  
Cell Infiltrate ◽  
H Pylori ◽  
The Relationship

The relationship between gastric inflammation caused byHelicobacter pyloriinfection and symptoms of dyspepsia remains controversial (1). Using a murine model of gastric infection, Bercik et al provide new insights into the mechanism underlying such interactions. Gastric sections from Balb/c mice infected withH pylori, strain SS-1, were used for both histological evaluation and studies of neuromuscular physiology. Acute infection (two weeks) caused an antral-predominant polymorphonuclear cell infiltrate that was superceded by a corpus-predominant mononuclear and macrophage infiltrate in chronic infection (three to 16 months).

scholarly journals A Conventional Beagle Dog Model for Acute and Chronic Infection with Helicobacter pylori

1999 ◽  
Vol 67 (6) ◽  
pp. 3112-3120 ◽  
Author(s):  
Giacomo Rossi ◽  
Michela Rossi ◽  
Claudia G. Vitali ◽  
Damiano Fortuna ◽  
Daniela Burroni ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Malt Lymphoma ◽  
Chronic Infection ◽  
Acute Infection ◽  
Chronic Phase ◽  
Human Infection ◽  
Peptic Ulcers ◽  
Treatment And Prevention ◽  
History Of ◽  
H Pylori

ABSTRACT Helicobacter pylori has been widely recognized as an important human pathogen responsible for chronic gastritis, peptic ulcers, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphoma. Little is known about the natural history of this infection since patients are usually recognized as having the infection only after years or decades of chronic disease. Several animal models ofH. pylori infection, including those with different species of rodents, nonhuman primates, and germ-free animals, have been developed. Here we describe a new animal model in which the clinical, pathological, microbiological, and immunological aspects of human acute and chronic infection are mimicked and which allows us to monitor these aspects of infection within the same individuals. Conventional Beagle dogs were infected orally with a mouse-adapted strain of H. pylori and monitored for up to 24 weeks. Acute infection caused vomiting and diarrhea. The acute phase was followed by polymorphonuclear cell infiltration, interleukin 8 induction, mononuclear cell recruitment, and the appearance of a specific antibody response against H. pylori. The chronic phase was characterized by gastritis, epithelial alterations, superficial erosions, and the appearance of the typical macroscopic follicles that in humans are considered possible precursors of MALT lymphoma. In conclusion, infection in this model mimics closely human infection and allows us to study those phases that cannot be studied in humans. This new model can be a unique tool for learning more about the disease and for developing strategies for treatment and prevention.

scholarly journals Natural Competence Promotes Helicobacter pylori Chronic Infection

2012 ◽  
Vol 81 (1) ◽  
pp. 209-215 ◽  
Author(s):  
Marion S. Dorer ◽  
Ilana E. Cohen ◽  
Tate H. Sessler ◽  
Jutta Fero ◽  
Nina R. Salama
Keyword(s):  
Helicobacter Pylori ◽  
Chronic Infection ◽  
Acute Infection ◽  
Host Cells ◽  
High Rate ◽  
Natural Competence ◽  
Content Type ◽  
Type Iv ◽  
Competence Factor ◽  
H Pylori

Animal models are important tools for studies of human disease, but developing these models is a particular challenge with regard to organisms with restricted host ranges, such as the human stomach pathogenHelicobacter pylori. In most cases,H. pyloriinfects the stomach for many decades before symptoms appear, distinguishing it from many bacterial pathogens that cause acute infection. To model chronic infection in the mouse, a human clinical isolate was selected for its ability to survive for 2 months in the mouse stomach, and the resulting strain, MSD132, colonized the mouse stomach for at least 28 weeks. During selection, thecagYcomponent of the Cag type IV secretion system was mutated, disrupting a key interaction with host cells. Increases in both bacterial persistence and bacterial burden occurred prior to this mutation, and a mixed population ofcagY+andcagYmutant cells was isolated from a single mouse, suggesting that mutations accumulate during selection and that factors in addition to the Cag apparatus are important for murine adaptation. Diversity in both alleles and genes is common inH. pyloristrains, and natural competence mediates a high rate of interstrain genetic exchange. Mutations of the Com apparatus, a membrane DNA transporter, and DprA, a cytosolic competence factor, resulted in reduced persistence, although initial colonization was normal. Thus, exchange of DNA between genetically heterogeneousH. pyloristrains may improve chronic colonization. The strains and methods described here will be important tools for defining both the spectrum of mutations that promote murine adaptation and the genetic program of chronic infection.

scholarly journals Non-helical Helicobacter pylori show altered gland colonization and elicit less gastric pathology during chronic infection

2018 ◽  
Author(s):  
Laura E Martinez ◽  
Valerie P O'Brien ◽  
Christina Leverich ◽  
Sue E Knoblaugh ◽  
Nina R Salama
Keyword(s):  
Helicobacter Pylori ◽  
Post Infection ◽  
Chronic Infection ◽  
Cell Shape ◽  
Quantitative Imaging ◽  
Acute Infection ◽  
Wild Type ◽  
Tissue Interactions ◽  
Colony Forming Units ◽  
H Pylori

Half of all humans harbor Helicobacter pylori in their stomachs. Helical cell shape is thought to facilitate H. pylori's ability to bore into the protective mucus layer in a corkscrew-like motion, thus enhancing colonization of the stomach. H. pylori cell shape mutants show impaired colonization of the mouse stomach, highlighting the importance of cell shape in infection. To gain a deeper understanding of how helical cell morphology promotes host colonization by H. pylori, we used 3D-confocal microscopy to visualize the clinical isolate PMSS1 and an isogenic straight rod mutant (Dcsd6) within thick longitudinal mouse stomach sections and performed volumetric image analysis to quantify the number of bacteria residing within corpus and antral glands in addition to measuring total colony forming units (CFU). We found that straight rods show attenuation during acute colonization of the stomach (one day or one week post-infection) as measured by total CFU. Our quantitative imaging revealed that wild-type bacteria extensively colonized antral glands at one week post-infection, while csd6 mutants showed variable colonization of the antrum at this timepoint. During chronic infection (one or three months post-infection), total CFU were highly variable, but similar for wild-type and straight rods. Both wild-type and straight rods persisted and expanded in corpus glands during chronic infection. However, the straight rods showed reduced inflammation and disease progression. Thus, helical cell shape contributes to tissue interactions that promote inflammation during chronic infection, in addition to facilitating niche acquisition during acute infection.

scholarly journals The correlation between lncRNAs and Helicobacter pylori in gastric cancer

2019 ◽  
Vol 77 (9) ◽  
Author(s):  
Narges Dastmalchi ◽  
Seyed Mahdi Banan Khojasteh ◽  
Mirsaed Miri Nargesi ◽  
Reza Safaralizadeh
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Molecular Mechanisms ◽  
Gastrointestinal Diseases ◽  
Mechanisms Of Action ◽  
Molecular Pathways ◽  
Gastric Diseases ◽  
Non Coding Rnas ◽  
H Pylori ◽  
The Relationship

ABSTRACT Helicobacter pylori infection performs a key role in gastric tumorigenesis. Long non-coding RNAs (lncRNAs) have demonstrated a great potential to be regarded as effective malignancy biomarkers for various gastrointestinal diseases including gastric cancer (GC). The present review highlights the relationship between lncRNAs and H. pylori in GC. Several studies have examined not only the involvement of lncRNAs in H. pylori-associated GC progression but also their molecular mechanisms of action. Among the pertinent studies, some have addressed the effects of H. pylori infection on modulatory networks of lncRNAs, while others have evaluated the effects of changes in the expression level of lncRNAs in H. pylori-associated gastric diseases, especially GC. The relationship between lncRNAs and H. pylori was found to be modulated by various molecular pathways.

scholarly journals Helicobacter pylori and Metabolic Diseases

2020 ◽  
Vol 20 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Sung Eun Kim
Keyword(s):  
Helicobacter Pylori ◽  
Fatty Liver Disease ◽  
Metabolic Diseases ◽  
Gastrointestinal Disorders ◽  
Systemic Effects ◽  
Peptic Ulcers ◽  
Alcoholic Fatty Liver ◽  
H Pylori ◽  
The Relationship ◽  
Alcoholic Fatty Liver Disease

<i>Helicobacter pylori</i> (<i>H. pylori</i>) is one of the most common pathogens that can cause certain gastrointestinal disorders, such as gastritis, peptic ulcers, and gastric cancer. Recently, interest in the systemic effects of <i>H. pylori</i> on extragastric manifestations is increasing. Representative diseases include hematologic, cardiovascular, neurodegenerative, autoimmune, dermatologic, allergic, hepatobiliary, and metabolic diseases. Among them, since the prevalence of metabolic diseases is on the rise worldwide, the relationship between <i>H. pylori</i> infection and metabolic diseases has become an interesting research issue. Many studies have been conducted to clarify any association. However, the results of those studies still remain controversial. This review focuses on recently published studies to investigate the relationship between <i>H. pylori</i> infection and metabolic diseases, including diabetes mellitus, metabolic syndrome, obesity, and non-alcoholic fatty liver disease, and their associated pathophysiology.

scholarly journals Dynamics of Lewis b Binding and Sequence Variation of the babA Adhesin Gene during Chronic Helicobacter pylori Infection in Humans

mBio ◽  
2014 ◽  
Vol 5 (6) ◽  
Author(s):  
Sandra Nell ◽  
Lynn Kennemann ◽  
Sandra Schwarz ◽  
Christine Josenhans ◽  
Sebastian Suerbaum
Keyword(s):  
Helicobacter Pylori ◽  
Amino Acid ◽  
Outer Membrane ◽  
Chronic Infection ◽  
Human Infection ◽  
Complete Loss ◽  
Blood Group Antigen ◽  
Content Type ◽  
Strain Pair ◽  
H Pylori

ABSTRACTHelicobacter pyloriundergoes rapid microevolution during chronic infection, but very little is known about how this affects host interaction factors. The best-studied adhesin ofH. pyloriis BabA, which mediates binding to the blood group antigen Lewis b [Le(b)]. To study the dynamics of Le(b) adherence during human infection, we analyzed pairedH. pyloriisolates obtained sequentially from chronically infected individuals. A complete loss or significant reduction of Le(b) binding was observed in strains from 5 out of 23 individuals, indicating that the Le(b) binding phenotype is quite stable during chronic human infection. Sequence comparisons ofbabAidentified differences due to mutation and/or recombination in 12 out of 16 strain pairs analyzed. Most amino acid changes were found in the putative N-terminal extracellular adhesion domain. One strain pair that had changed from a Le(b) binding to a nonbinding phenotype was used to study the role of distinct sequence changes in Le(b) binding. By transformations of the nonbinding strain with ababAgene amplified from the binding strain,H. pyloristrains with mosaicbabAgenes were generated. Recombinants were enriched for a gain of Le(b) binding by biopanning or for BabA expression on the bacterial surface by pulldown assay. With this approach, we identified several amino acid residues affecting the strength of Le(b) binding. Additionally, the data showed that the C terminus of BabA, which is predicted to encode an outer membrane β-barrel domain, plays an essential role in the biogenesis of this protein.IMPORTANCEHelicobacter pyloricauses a chronic infection of the human stomach that can lead to ulcers and cancer. The bacterium can bind to gastric epithelial cells with specialized outer membrane proteins. The best-studied protein is the BabA adhesin which binds to the Lewis b blood group antigen. SinceH. pyloriis a bacterium with very high genetic variability, we asked whetherbabAevolves during chronic infection and how mutations or recombination inbabAaffect binding. We found that BabA-mediated adherence was stable in most individuals but observed a complete loss of binding or reduced binding in 22% of individuals. One strain pair in which binding was lost was used to generatebabAsequences that were mosaics of a functional allele and a nonfunctional allele, and the mosaic sequences were used to identify amino acids critically involved in binding of BabA to Lewis b.

Interaction of 22 risk SNPs with Helicobacter pylori infection and risk of gastric cardia adenocarcinoma

2019 ◽  
Vol 15 (31) ◽  
pp. 3579-3585 ◽  
Author(s):  
Fan-Kai Xiao ◽  
Jian Xue Yang ◽  
Xin Min Li ◽  
Xue Ke Zhao ◽  
Peng Yuan Zheng ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Helicobacter Pylori Infection ◽  
Gastric Cardia ◽  
Gastric Cardia Adenocarcinoma ◽  
Susceptibility Loci ◽  
Single Nucleotide ◽  
Increased Risk ◽  
Risk Snps ◽  
H Pylori ◽  
The Relationship

Aim: To determine the prevalence of Helicobacter pylori infection and correlation between H. pylori infection and single nucleotide polymorphism (SNPs) identified in gastric cardia adenocarcinoma (GCA) patients. Methods: A case control study was performed. 22 risks of GCA-related SNPs were identified by genotyping assay and the relationship between susceptibility loci for GCA and H. pylori infection was further analyzed. Results: Helicobacter pylori infection was associated with GCA significantly (odds ratio: 1.40; 95% CI: 1.29–1.53 p < 0.01). Five GCA risk SNPs had their genotypes significantly different between H. pylori positive patients and H. pylori negative patients. Conclusion: The interaction between SNPs susceptibility loci and H. pylori infection is associated with an increased risk of GCA.

scholarly journals Development of a Tetracycline-Inducible Gene Expression System for the Study of Helicobacter pylori Pathogenesis

2013 ◽  
Vol 79 (23) ◽  
pp. 7351-7359 ◽  
Author(s):  
Aleksandra W. Debowski ◽  
Phebe Verbrugghe ◽  
Miriam Sehnal ◽  
Barry James Marshall ◽  
Mohammed Benghezal
Keyword(s):  
Helicobacter Pylori ◽  
Animal Models ◽  
Chronic Infection ◽  
Fluorescent Protein ◽  
Expression System ◽  
Content Type ◽  
Conditional Expression ◽  
H Pylori ◽  
Green Fluorescent

ABSTRACTDeletion mutants and animal models have been instrumental in the study ofHelicobacter pyloripathogenesis. Conditional mutants, however, would enable the study of the temporal gene requirement duringH. pyloricolonization and chronic infection. To achieve this goal, we adapted theEscherichia coliTn10-derived tetracycline-inducible expression system for use inH. pylori. TheureApromoter was modified by inserting one or twotetoperators to generate tetracycline-responsive promoters, nameduPtetO, and these promoters were then fused to the reportergfpmut2 and inserted into different loci. The expression of the tetracycline repressor (tetR) was placed under the control of one of three promoters and inserted into the chromosome. Conditional expression of green fluorescent protein (GFP) in strains harboringtetRanduPtetO-GFPwas characterized by measuring GFP activity and by immunoblotting. The twotet-responsiveuPtetOpromoters differ in strength, and induction of these promoters was inducer concentration and time dependent, with maximum expression achieved after induction for 8 to 16 h. Furthermore, the chromosomal location of theuPtetO-GFPconstruct and the nature of the promoter driving expression oftetRinfluenced the strength of theuPtetOpromoters upon induction. Integration ofuPtetO-GFPandtetRconstructs at different genomic loci was stablein vivoand did not affect colonization. Finally, we demonstrate tetracycline-dependent induction of GFP expressionin vivoduring chronic infection. These results open new experimental avenues for dissectingH. pyloripathogenesis using animal models and for testing the roles of specific genes in colonization of, adaptation to, and persistence in the host.

scholarly journals Effect of Helicobacter pylori Infection on Serum Lipid Profile

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Mohamadreza Haeri ◽  
Mahmoud Parham ◽  
Neda Habibi ◽  
Jamshid Vafaeimanesh
Keyword(s):  
Helicobacter Pylori ◽  
Lipid Profile ◽  
Blood Sugar ◽  
Serum Lipid ◽  
Density Lipoprotein ◽  
Population Data ◽  
Serum Lipid Profile ◽  
Significant Difference ◽  
H Pylori ◽  
The Relationship

Background. Some studies suggest a significant relationship between Helicobacter pylori infection and atherogenesis; but the mechanism of the relationship is almost unknown. The current study aimed at evaluating the relationship between H. pylori infection and serum lipid profile. Patients and Methods. The current study was conducted on 2573 patients, from 2008 to 2015. The serum anti-Helicobacter pylori antibody titer and serum lipid profile were assessed in the study population; data were statistically analyzed by SPSS version 16. P values < 0.05 were considered significant. Results. In the current study, 66.5% of the cases were serologically positive for H. pylori. Among male cases, the level of low density lipoprotein (LDL) was higher in patients with H. pylori infection, compared with that of the ones without the infection (P=0.03); although level of triglyceride (TG) was higher and the level of high density lipoprotein (HDL) was lower in the cases with H. pylori infection; there was no statistically significant difference between the cases with and without H. pylori infection regarding the level of HDL and TG. Among female cases, the level of TG was significantly lower in patients with H. pylori infection, compared with that of the ones without the infection (P=0.001); but there was no significant difference between the cases with and without H. pylori infection regarding the level of LDL and HDL. The mean fasting blood sugar (FBS) in the cases with H. pylori infection was significantly higher than that of the ones without the infection (P=0.04). Conclusion. According to the results of the current study, the levels of LDL and FBS were high among the male cases with H. pylori infection. However, in females with H. pylori infection the level of TG was low; hence, it seems that the atherogenicity of H. pylori affected the level of blood sugar more.

scholarly journals Involvement of CO2 generated by urease in multiplication of Helicobacter pylori

2021 ◽  
Vol 7 (3) ◽  
pp. 045-053
Author(s):  
Masaaki Minami ◽  
Shin-nosuke Hashikawa ◽  
Takafumi Ando ◽  
Hiroshi Kobayashi ◽  
Hidemi Goto ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Mutant Strain ◽  
Type Strain ◽  
Wild Type Strain ◽  
Neutral Medium ◽  
Wild Type ◽  
In The Wild ◽  
H Pylori ◽  
Carbon Dioxide Co2 ◽  
The Relationship

Helicobacter pylori (H. pylori) urease generates both ammonia (NH3) and carbon dioxide (CO2) from urea. NH3 helps H. pylori to survive in the stomach in part by neutralizing gastric acid. However, the relationship between CO2 and H. pylori is not completed cleared. We examined the effect of CO2 generated by urease on multiplication of H. pylori by using isogenic ureB mutant and ureB complemented strain from H. pylori strain JP26. Wild-type strain survived in the medium supplement with 1mM urea in room air, however, the urease negative strain did not. To discern whether CO2 was incorporated into H. pylori, 14C in bacillus was counted after 6 hours incubation with 14C urea in both acidic and neutral medium. Significant more 14C uptake was detected in wild-type strain compared to ureB mutant strain and this uptake in the wild-type strain was more under acidic condition compared to under neutral condition, but no difference was identified in the mutant strain. These results suggest that CO2 generated by urease plays a role in multiplication of H. pylori.

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