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 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.

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 Helicobacter Pylori Negative Extra-nodal Marginal Zone B Cell Lymphoma of Mucosa Associated Lymphoid Tissue (MALT) Type Following Roux-en-Y Gastric Bypass (RYGB)

2021 ◽  
Author(s):  
Zachary Eagle ◽  
Francis Essien ◽  
Kimberly Zibert ◽  
Charles Miller ◽  
Rina Eden ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Malt Lymphoma ◽  
Lymphoid Tissue ◽  
Marginal Zone ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Common Type ◽  
Gastric Malt Lymphoma ◽  
History Of ◽  
H Pylori

Gastric MALT lymphoma is a common type of non-Hodgkin’s lymphoma that has the potential for cure in patients found to have concomitant Helicobacter pylori infection.1,2 This case report explores the evaluation, diagnosis, and treatment of H. pylori negative MALT lymphoma in a patient with a history of a RYGB.

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).

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 MALT lymphoma: epidemiology, clinical diagnosis and treatment

2018 ◽  
Vol 11 (3) ◽  
pp. 187-193 ◽  
Author(s):  
Petruta Violeta Filip ◽  
◽  
Denisa Cuciureanu ◽  
Laura Sorina Diaconu ◽  
Ana Maria Vladareanu ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
B Cell ◽  
Malt Lymphoma ◽  
Cell Lymphoma ◽  
Gastric Lymphoma ◽  
Eradication Therapy ◽  
B Cell Lymphoma ◽  
Gastric Malt Lymphoma ◽  
H Pylori

Primary gastric lymphoma (PGL) represents a rare pathology, which can be easily misdiagnosed because of unspecific symptoms of the digestive tract. Histologically, PGL can vary from indolent marginal zone B-cell lymphoma of the mucosa-associated lymphoid tissue (MALT) to aggressive diffuse large B-cell lymphoma (DLBCL). During the years, clinical trials revealed the important role of Helicobacter pylori (H. pylori) in the pathogenesis of gastric MALT lymphoma. Infection with Helicobacter pylori is an influential promoter of gastric lymphomagenesis initiation. Long-term studies revealed that eradication therapy could regress gastric lymphomas.

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 Prevalence of vacA, cagA, and iceA Virulence Factors of Helicobacter Pylori Isolated from Gastro-duodenal Patients

2020 ◽  
Vol 14 (1) ◽  
pp. 72-79
Author(s):  
Ahmed Husham Salman ◽  
Aumed Arshad Hawezy
Keyword(s):  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Gastric Lymphoma ◽  
Signs And Symptoms ◽  
Molecular Technique ◽  
Peptic Ulcers ◽  
Back Ground ◽  
H Pylori ◽  
Pcr Test

Back ground: Helicobacter pylori are bacteria colonize in the human epithelial cells of the gastrointestinal tract. Its infection causes different diseases, including chronic gastritis, peptic ulcers, gastric lymphoma and adenocarcinoma. H. pylori have many virulence factors attributing in one or more biological functions. Objective: Detecting the prevalence of virulence factor genes vacA, cagA, iceA among strain of H. pylori using molecular technique (PCR). Materials and methods: Sixty patients (27 male and 33 female), aged 18 and above included in the present study who showed signs and symptoms of H. pylori, and undergo endoscopy between period of November 2019 and February 2020. RUT and PCR test done to detect the presence of H. pylori infection, also PCR used to detect the three virulence factors. Results: Result showed that 44 patients, 21 (47.7%) male and 23 (52.3%) female were detected as positive H. pylori infections, among them 13 (29.5%) above 50 years, and 31 (70.4%) were below 50 years. While prevalence of the virulence factors vacA, cagA, and iceA were (100%), (84.1%), and (34.1%) respectively. Conclusion: It can be concluded that the frequency and prevalence of these genes are differed and showed significant differences among them. Also, PCR test is sensitive and accurate for detection of H. pylori virulence genes.

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.

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