scholarly journals Helicobacter pylori as a crucial factor in intestinal metaplasia development of gastric mucosa

2016 ◽  
Vol 2 (3) ◽  
pp. 173
Author(s):  
Sergii Vernygorodskyi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Intestinal Metaplasia ◽  
Chronic Atrophic Gastritis ◽  
Gastric Epithelium ◽  
Number Of Genes ◽  
Activating Transcription Factor ◽  
H Pylori ◽  
Gene Inhibition

<p class="BodyText1"><em>Helicobacter pylori</em> (<em>H. pylori</em>) is detected on the surface of gastric epithelium and in goblet cells, predominantly in patients with chronic atrophic gastritis and incomplete intestinal metaplasia (IM). <em>H. pylori</em> infection persistence leads to the formation of gastrointestinal phenotype of IM. <em>H. pylori</em> can be considered as an etiological factor of IM. It inhibits the expression of SOX2 in gastric epithelial cells, hence activating transcription factor CDX2 as a counterpart to <em>MUC5AC</em> gene inhibition and <em>MUC2</em> gene induction. Thus, in metaplastic cells, programming differentiation after intestinal phenotype will develop. The role of <em>H. pylori</em> in the origin of intestinal metaplasia of gastric mucosa was defined in this study to elucidate the probable mechanism of cell reprogramming. The activation of CDX2, with simultaneous inactivation and decreased number of genes (<em>e.g.</em>, <em>SHH</em>, <em>SOX2</em>, and <em>RUNX3</em>) responsible for gastric differentiation, was identified to cause the appearance of IM. </p>

scholarly journals Prevalence of barrett's esophagus, its relationship with chronic Helicobacter pylori-associated gastritis, atrophy and metaplasia of gastric mucosa

2019 ◽  
Vol 2 (8) ◽  
pp. 77-89
Author(s):  
T.V. Serha ◽  
O.G. Kuryk ◽  
V.A. Yakovenko ◽  
G.A. Solovyova ◽  
R.P. Tkachenko
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Intestinal Metaplasia ◽  
Barrett’S Esophagus ◽  
Histological Examination ◽  
Barrett's Esophagus ◽  
Gastric Epithelium ◽  
Gastric Type ◽  
H Pylori ◽  
Epithelial Metaplasia

The aim - to identify the frequency of Helicobacter pylori infection, atrophic and metaplastic changes in the gastric mucosa in patients with Barrett's esophagus. Materials and methods. A retrospective study of 7392 cases of complex esophagogastroscopy with a biopsy of the epithelium of the mucous membrane of the esophagus and stomach, followed by a morphological study, was conducted on the basis of the Medical Centre “Oberig” clinic for the period 2010-2018. Statistical data was performed using the MedStat package. To assess the prevalence of changes in the esophagus and stomach, a 95% confidence interval was calculated using the Fisher angular transformation method. The probability of differences between group averages and relative values ​​was determined using the method of parametric statistics by calculating the t-Student criterion. The difference between the average values ​​was considered significant at p <0.05. To compare the frequencies in different groups, the Pearson chi-square test was used. Results. Endoscopically cylindrical columnar metaplasia of the esophagus epithelium was detected in 2994 patients (40.5% CI 39.4% -41.6% at a significance level of p = 0.05). In a histological examination, esophageal epithelial metaplasia was confirmed in 2910 patients (39.4% CI 38.3%-40.5%). 876 cases of gastric-type esophagus epithelial metaplasia were diagnosed (30.1%, CI 28.4-31.5%); 2034 cases of intestinal type metaplasia (69.9%, CI 68.2-71.6%). Histological examination of biopsy samples of the gastric mucosa in 5640 (76.3%, CI 75.3-77.3%) patients revealed atrophy of the gastric mucosa. In 2532 cases (34.3%, CI 33.2-35.3%), complete and incomplete intestinal metaplasia of the gastric epithelium was diagnosed. In 4524 (61.2%, CI 60.1-62.3%) patients, Helicobacter pylori was detected. In the presence of H. pylori, gastric esophageal epithelial metaplasia was detected in 510 of 3558 (14.3%, CI 13.2-15.5%, p = 0.05), intestinal metaplasia of the esophagus epithelium - in 966 of 4014 (24.1% CI 22.8 -25.4%, p = 0.05). Conclusion. Esophageal epithelial metaplasia is a common pathology, accounting for 39.4% among patients who underwent esophagogastroscopy. The presence of a strong connection between intestinal metaplasia of the epithelium of the esophagus and atrophy of the gastric mucosa with intestinal metaplasia of the epithelium of the stomach was found. Esophageal epithelial metaplasia is significantly less common with Helicobacter pylori gastritis, therefore the presence of H. pylori has a protective effect on the occurrence of esophageal epithelial metaplasia.

scholarly journals Mechanisms of interacting Helicobacter pylori with gastric mucosal epithelium. II. A reaction of gastric epithelium on Helicobacter pylori colonization and persistence

2019 ◽  
Vol 9 (2) ◽  
pp. 253-261
Author(s):  
O. K. Pozdeev ◽  
A. O. Pozdeeva ◽  
Yu. V. Valeeva ◽  
P. E. Gulyaev ◽  
A. N. Savinova
Keyword(s):  
Helicobacter Pylori ◽  
T Cell ◽  
Epithelial Cell ◽  
Gastric Mucosa ◽  
Mapk Pathway ◽  
Bacterial Colonization ◽  
Gastric Epithelium ◽  
T Cell Subsets ◽  
H Pylori ◽  
Apoptotic Factors

Gastric and duodenal recurrent inflammatory diseases have a high prevalence, but the role played by microbes in its development remained unclear. However, the data published in 1983 by Marshall and Warren about isolatingHelicobacter pylorifrom the stomach mucosa of the patient with gastritis and proposing relevant cultivation methods was the turning point in investigating etiology of the upper digestive tract inflammatory disorders. Moreover, it was shown that the majority ofH. pylorispp. are found within the gastric lumen upon colonization, whereas around 20% of them are attached to the epithelial cells in the stomach. In addition, effects of interacting H. pylori with gastric epithelium and activation of some defense mechanisms due to bacterial colonization and spreading were analyzed. It was found that along with triggering pro-inflammatory response induced by proteins VacA as well as phosphorylated/unphosphorylated CagA, wherein the latter is able to induce a set of protective reactionsH. pyloridisrupts intercellular contacts, affects epithelial cell polarity and proliferation, and activates SHP-2 phosphatase resulting in emerging diverse types of cellular responses. The activation mechanisms for the mitogen-activated protein kinase (MAPK) pathway were discussed. The ability ofH. pylorito regulate apoptosis, particularly via its suppression, by expressing ERK kinase and protein MCL1 facilitating bacterial survival in the gastric mucosa as well as beneficial effects related to bacterial circulation on gastric epithelial cell survival elicited by anti-apoptotic factors were also examined. Of note, persistence of H. pylori are mainly determined by activating transcriptional factors including NF-κB, NFAT, SRF, T-cell lymphoid enhancing factor (TCF/LEF), regulating activity of MCL1 protein, in turn, being one of the main anti-apoptotic factors, as well as induced production of the migration inhibitory factor (MIF). The role of VacA cytotoxin in triggering epithelial cell apoptosis via caspase-mediated pathways was also considered. Infection withH. pyloriis accompanied by release of proinflammatory cytokine cocktail detected bothin vitroandin vivo. In particular, bacterial urease activating transcriptional factor NF-κB was shown to play a crucial role in inducing cytokine production. Moreover, such signaling pathways may be activated afterH. pyloriis attached to the cognate receptor in the gastric epithelial surface by interacting with CD74 and MHC class II molecules. Finally, a role for various CD4+T cell subsets, particularly type 17 T helper cells (Th17) in inducing immune response against H. pylori antigens in gastric mucosa was revealed were also discussed. 

scholarly journals Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

2021 ◽  
Author(s):  
Ghorbanali Rahimian ◽  
Milad Shahini Shams Abadi ◽  
Reza Ahmadi ◽  
Mohammedhadi Shafigh ◽  
Fatemeh Azadegan-Dehkordi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Treg Cells ◽  
Infected Group ◽  
Ulcer Disease ◽  
Tnf Α ◽  
H Pylori ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Helicobacter pylori (H. pylori) -induced gastric inflammation in the gastric mucosa and significantly increases the risk of developing gastritis and peptic ulcer disease (PUD). The objective of this research is to determine the role of tumor necrosis factor-α (TNF-α) expression in the gastric mucosa of patients with H. pylori –associated gastritis and PUD compared to uninfected patients, and we determined the relation between TNF-α expression and Th1/Th17/Th22, and Treg cells.Methods: Fifty-five patients with H. pylori –associated gastritis, 47 patients with H. pylori –associated PUD, and 48 uninfected patients were in this research. Antrum biopsy was used to detect H. pylori, virulence factors and histopathological assessments.Results: Expression of TNF-α in the infected group was significantly higher than the uninfected group. Also, cagA/oipA-positive infected patients induce significantly more TNF-α expression than do cagA/oipA-negative infected patients. Expression of TNF-α was significantly increased in the PUD group than the gastritis group. Notably, TNF-α expression had a significant positive correlation with the frequency of Th1/Th17/Th22 lymphocytes in the PUD group.Conclusion: These findings indicate the importance of increasing TNF-α with Th1, Th17, Th22 responses increase as an important risk factor for PUD in context of H. pylori infection.

scholarly journals Helicobacter pylori infection and inflammatory bowel diseases

2021 ◽  
Vol 11 (1) ◽  
pp. 68-78
Author(s):  
Yu. P. Uspenskiy ◽  
N. V. Baryshnikova ◽  
A. N. Suvorov ◽  
A. V. Svarval
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Inflammatory Bowel Diseases ◽  
Pathogenic Bacteria ◽  
T Cell Response ◽  
Aminosalicylic Acid ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
H Pylori

Helicobacter pylori is detected in the human intestine on average in 35% of clinical cases, but the question about its etiopathogenetic role in intestinal diseases has not been fully investigated. Many scientists study a relationship between the H. pylori persistence and development of various bowel diseases. Diverse viewpoints have been proposed regarding a potential link between H. pylori and inflammatory bowel diseases (IBD). Here we review the data from domestic and foreign studies aimed at examining potential role of H. pylori both as a trigger and protector resulting in the pathogenetic alterations leading to developing Crohn‘s disease and ulcerative colitis. The former is favored by the hypothesis wherein H. pylori may trigger IBD due to potential connection between extragastric infection and its direct damaging action as well as indirect effects contributing to the initiation of oxidative stress, autoimmune aggression and development of intestinal dysbiosis. In addition, the effects of enterohepatic Helicobacter spp. promoting IBD pathogenesis are discussed. The mechanisms underlying the protective role of H. pylori infection may be driven via differentially expressed acute and/or chronic local inflammatory mucosal response able to downmodulate systemic immune responses and suppress autoimmune reactions, as well as skewing host immune response from a pro-inflammatory Th1/Th17 cell-mediated towards regulatory T-cell response. Moreover, it was found that H. pylori may induce production of antibacterial peptides counteracting potentially pathogenic bacteria involved in IBD pathogenesis. In particular, it was found that IBD patients are dominated with moderate active antral gastritis coupled to atrophy, with the peak intensity observed in patients under 30 years of age. Intensity of intestinal metaplasia in the gastric mucosa of IBD patients accounted for by the duration of the disease course. Basal IBD therapy with 5-aminosalicylic acid lowers severity and activity of gastritis, degree of atrophy as well as magnitude H. pylori invasion in the gastric mucosa. There is evidence that 5-aminosalicylic acid-containing drugs may result in a so-called “spontaneous eradication” of H. pylori infection. Extended investigations are required to examine a role of H. pylori in IBD pathogenesis.

Intrafamilial Infection of Helicobacter Pylori: Abnormal Gastric Epithelial Cells, Pedestal-Rich H. Pylori Adherence, and a Gene Mutation in a Child with Protein-Losing Gastroenteropathy

2019 ◽  
Vol 2 (3) ◽  
pp. 83-99
Author(s):  
T.W. Wan ◽  
O. Khokhlova ◽  
W. Higuchi ◽  
I. Protasova ◽  
Olga V. Peryanova ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Gene Mutation ◽  
Virulence Factor ◽  
East Asian ◽  
Gastric Epithelium ◽  
Gastric Epithelial Cells ◽  
H Pylori

Abstract Helicobacter pylori, one of the most prevalent human pathogens, colonizes the gastric mucosa and is associated with gastric diseases, such as gastritis and peptic ulcers, and is also a bacterial risk factor for gastric cancer. Cytotoxin-associated gene A (CagA) protein, a major virulence factor of H. pylori, is phosphorylated in cells at its Glu-Pro-IIe-Tyr-Ala (EPIYA) motif and is considered to trigger gastric cancer. CagA is classified into two forms, Western CagA with EPIYA-ABC and East Asian CagA with EPIYA-ABD, with the latter associated with a high risk of developing gastric cancer. CagA causes morphological transformation of cells, yielding the “hummingbird” phenotype in AGS cells and possibly membranous pedestals in the gastric epithelium, albeit rarely. H. pylori adherence to the gastric mucosa is not yet fully understood. Here, we describe an intrafamilial infection case of H. pylori, focusing on the gastric epithelium, H. pylori adherence, and a gene mutation in a child with protein-losing gastroenteropathy (characterized by excessive loss of plasma proteins into the gastrointestinal tract). H. pylori, which also infected family members (mother and father), was genetically a single clone with the virulence genes of an East Asian type. The patient’ gastric mucosa exhibited some unique features. Endoscopy revealed the presence of protein plugs on the mucosal surface, which were immunoelectrophoretically similar to serum proteins. Electron microscopy revealed abnormal gastric epithelial cells, totally covered with the secretions or possessing small swollen structures and irregular microvilli. The patient’s H. pylori infection was characterized by frequently occurring thick pedestals, formed along adherent H. pylori. The serum protein level returned to normal and the protein plugs disappeared after the successful eradication of H. pylori, albeit with lag periods for healing. He had a mutation in the OCRL1 gene, associated with Dent disease (asymptomatic proteinuria). Thus, in the patient’s gastric mucosa, we found the abnormal gastric epithelial cells, which may be caused by an OCRL1 mutation or H. pylori, and pedestal-rich H. pylori infection, possibly caused by a higher level of action of CagA in the abnormal epithelial cells. The data suggests a novel H. pylori virulence factor associated with “excessive plasma protein release”.

scholarly journals Role of apoptosis induced by Helicobacter pylori infection in the development of duodenal ulcer

Gut ◽  
1999 ◽  
Vol 44 (4) ◽  
pp. 456-462 ◽  
Author(s):  
K Kohda ◽  
K Tanaka ◽  
Y Aiba ◽  
M Yasuda ◽  
T Miwa ◽  
...  
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Clinical Stage ◽  
Endoscopic Examination ◽  
Gastric Epithelium ◽  
Antral Mucosa ◽  
Biopsy Specimens ◽  
A Cell ◽  
H Pylori

BACKGROUNDHelicobacter pylori affects gastric epithelium integrity by acceleration of apoptosis. However, it remains unclear what product of the bacteria causes apoptosis, or whether or not the apoptosis is involved in the development of ulcers.AIMSTo elucidate the factor from H pylori that causes acceleration of apoptosis and the role of apoptosis in the development of duodenal ulcer in H pylori infection.PATIENTSFiveH pylori negative healthy volunteers, 47H pylori positive patients with duodenal ulcer, and 35 H pylori positive patients with gastric ulcer.METHODSAn endoscopic examination was carried out to diagnose ulcers and determine their clinical stage. To analyse apoptosis, a cell cycle analysis was performed using biopsy specimens.RESULTSThere was a significant correlation between the urease activity of theH pylori strain and the level of apoptosis induced by this bacterial strain. Moreover, in duodenal ulcer patients infected with H pylori, the patients with an active ulcer exhibited a significantly higher level of apoptosis than those with ulcers at both the healing and scarring stages.CONCLUSIONThese findings suggest that acceleration of apoptosis in the antral mucosa caused by the urease of H pylori plays a crucial role in the development of ulcers in the duodenum.

scholarly journals State of lipid peroxidation and antioxidant defense in chronic gastritis associated with Helicobacter pylori-infection in middle-aged males

2020 ◽  
Vol 10 (4) ◽  
pp. 741-746
Author(s):  
O. V. Smirnova ◽  
A. A. Sinyakov ◽  
N. M. Titova
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Antioxidant Defense ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Metabolism Enzymes ◽  
H Pylori

Helicobacter pylori is the most widespread human pathogen, with prevalence reaching up to 20—40% and 80— 90% of adult infection in developed and developing countries, respectively. Many authors consider this infection as a major factor in the development of gastric cancer. In case of H. pylori infection, free homogeneous oxidation is augmented, that elevates the blood amount of POL products. Hyperproduction of reactive oxygen species stimulates free radical POL, accompanied by membrane destruction, damage to proteins, lipids, and DNA. Thus, the destruction of the intracellular and cell outer membranes occurs resulting in cell death. In diseases associated with H. pylori infection, there is a dysregulation of the lipid peroxidation system — antioxidant defense contributing to inconsistency in the regeneration phases triggering disease progression. The aim of our work was to study indicators of POL (diene conjugates, malonic dialdehyde) and antioxidant protection (AOP) (superoxide dismutase enzymes, catalase) in chronic gastritis and chronic atrophic gastritis associated with H. pylori infection. In patients with CG associated with H. pylori as well as CAG and CAG associated with H. pylori they were featured with increased amount of primary (↑DC) and end TBA-active products of lipid peroxidation (↑MDA), whereas activity of superoxide dismutase was decreased, additionally highlighted with reduced catalase activity (↑CAT) in CAG and CAG associated with H. pylori. H. pylori just triggers the mechanisms of ROS generation in host cells. The energy of redox reactions is used by the microorganism to carry out its physiological functions and serves as a factor in its own pathogenicity, the ROS generated in such reactions can have a damaging effect on the structure of gastric mucosa. In addition, examining H. pylori genome has shown that it bears the genes encoding oxidative metabolism enzymes, such as SOD, catalase, nitroreductase, flavodoxin oxidoreductase. Long-term persistence of H. pylori in the gastric mucosa paralleled with its increased biomass accounts for it being the main source of ROS production able to augment lipid peroxidation and cause damage to the membrane structures and DNA of gastric epithelium cells.

scholarly journals Review of Research on Routes of Helicobacter pylori Infection

2015 ◽  
Vol 4 (2) ◽  
pp. 45-49
Author(s):  
Hang Li
Keyword(s):  
Helicobacter Pylori ◽  
Drinking Water ◽  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Gastric Adenocarcinoma ◽  
Precancerous Lesions ◽  
Natural Environments ◽  
H Pylori

AbstractIn recent years, many scholars conducted in-depth research onHelicobacter pyloriand identified it as an important pathogen of chronic gastritis and peptic ulcer.H. pylorialso causes also and contributes to precancerous lesions (atrophic gastritis and intestinal metaplasia) and is closely related to occurrence and development of gastric adenocarcinoma and gastric mucosa-associated lymphoma. This study summarizes biological characteristics, epidemic status, and infection route ofH. pyloriand reviews research on roles of natural environments, especially drinking water, during infection.

scholarly journals Chronic gastritis and carcinogenesis issues

2019 ◽  
Vol 45 (4) ◽  
pp. 65-70
Author(s):  
M. M. Karimov ◽  
G. N. Sobirova ◽  
U. K. Abdullayeva
Keyword(s):  
Gastric Cancer ◽  
Intestinal Metaplasia ◽  
Chronic Atrophic Gastritis ◽  
Precancerous Conditions ◽  
Increased Risk ◽  
Operated Stomach ◽  
Increasing Risk ◽  
H Pylori ◽  
Definition Of

Risk factors contributing to the transformation of chronic atrophic gastritis into gastric cancer are analyzed. Detection and monitoring of patients with precancerous conditions/lesions (precancerous changes), proper screening of H. pylori make early diagnosis of gastric cancer real. Features of precancerous conditions are given in order of increasing risk of developing gastric cancer. Adenomatous polyps of the stomach take the first place. Subsequent precancerous conditions include: cancer of the operated stomach, Menetria disease (hypertrophic gastropathy), B12-deficient anemia, and gastric ulcer. A definition of intestinal metaplasia subtypes is proposed as a risk factor for gastric cancer, dividing into complete and incomplete one, taking into account reduction in the expression of gastric mucins MUC1, MUC5AC and MUC6. Currently, the development of gastric cancer (mainly of the “intestinal type”) is considered as a multistage process involving the sequence of mucosal change, such as chronic inflammation, atrophy, intestinal metaplasia, dysplasia and adenocarcinoma. Role of the organism’s genetic susceptibility to H. pylori infection, factors of pathogenicity contributing to epithelial metaplasia, are analyzed. Role of Toll-like type 4 receptors (TLR4) involved in the recognition of H. pylori is clarified. It is with this type of receptors that the development of an excessive immune response of the host is associated, resulting in damage to the mucous membrane in H. pylori-infected individuals. In particular, carriers of TLR4+896A> G polymorphism have a more severe atrophy of the stomach and degree of inflammation, as well as an increased risk of non-cardiac gastric cancer.

The Role of E-cadherin in Helicobacter pylori-Related Gastric Diseases

2019 ◽  
Vol 20 (1) ◽  
pp. 23-28
Author(s):  
Yunzhan Zhang ◽  
Danyan Li ◽  
Yunkai Dai ◽  
Ruliu Li ◽  
Yong Gao ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Precancerous Lesions ◽  
Research Literature ◽  
Gastric Diseases ◽  
H Pylori ◽  
The Relationship ◽  
E Cadherin

Background: Helicobacter pylori (H. pylori)-related gastric diseases are a series of gastric mucosal disorders associated with H. pylori infection. Gastric cancer (GC) is widely believed to evolve from gastritis and gastric ulcer. As an important adhesion molecule of epithelial cells, E-cadherin plays a key role in the development of gastric diseases. In this review, we aim to seek the characteristic of E-cadherin expression at different stages of gastric diseases. Methods: We searched plenty of databases for research literature about E-cadherin expression in H. pylori-related gastric diseases, and reviewed the relationship of E-cadherin and H. pylori, and the role of E-cadherin at different stages of gastric diseases. Results: H. pylori was shown to decrease E-cadherin expression by various ways in vitro, while most of clinical studies have not found the relationship between H. pylori and E-cadherin expression. It is defined that poor outcome of GC is related to loss expression of E-cadherin, but it is still unclear when qualitative change of E-cadherin expression in gastric mucosa emerges. Conclusion: Expression level of E-cadherin in gastric cells may be a consequence of injury factors and body’s selfrepairing ability. More studies on E-cadherin expression in gastric mucosa with precancerous lesions need to be performed, which may be potential and useful for early detection, prevention and treatment of GC.

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