scholarly journals Role of genetic structure of Helicobacter Pylori in formation of chronic inflammatory process in gastric mucosa

2021 ◽  
Vol 38 (1) ◽  
pp. 87-99
Author(s):  
O. M. Manyakina ◽  
I. S. Akkuratova-Maksimova ◽  
T. G. Pukhova ◽  
A. S. Shitova
Keyword(s):  
Helicobacter Pylori ◽  
Genetic Structure ◽  
Gastric Mucosa ◽  
Inflammatory Process ◽  
Gastric Glands ◽  
Highly Pathogenic ◽  
Genetic Characteristics ◽  
Chronic Inflammatory Process ◽  
Barr Virus

The literature review highlights the questions of the interaction of Helicobacter pylori and the human body. Modern data on the structure of the pathogenicity island in the Helicobacter pylori genome are presented. There is given a detailed description of both well-known virulence and pathogenicity factors of the infection (genes encoding the formation of urease subunits, in particular urel, cytotoxin associated gene A, vacuolating cytotoxin gen A, blood group associated binding adhesion, induced by contact with epithelium) and less studied ones (sialic acid-binding adhesion, adhesion-associated lipoprotein A and B, adhesin gene of Helicobacter pylori, Hp outer membrane protein). The significance of individual genes and proteins encoded by them in the development of chronic inflammatory process in diseases of the upper digestive tract, as well as in ulcer and carcinogenesis is analyzed. Mechanisms of interaction of bacteria with epithelial cells of the gastric mucosa, adhesive and cytotoxic effects of Helicobacter pylori, factors of biofilm formation are described. The influence of the genetic structure of Infect on cytological composition of the gastric glands in the form of reduction of specialized glandular cells chief and parietal cells of pyloric glands and the increase of endocrine cells in the pool is assessed. It is shown that colonization of the gastric mucosa by highly pathogenic strains of Helicobacter pylori contributes to the development of widespread pronounced and active inflammation in it, the appearance of morphological signs of atrophy. The role of the genetic characteristics of the infection in the failure of anti-helicobacter therapy is emphasized. Separately, the question of the effect of combined infection of the gastric mucosa with highly pathogenic strains of Helicobacter pylori and Epstein-Barr virus is highlighted.

scholarly journals Influence of genetic characteristics of Helicobacter pylori on pathomorphology of gastric mucosa in young persons with chronic gastritis

2021 ◽  
Vol 37 (6) ◽  
pp. 42-47
Author(s):  
E. M. Spivak ◽  
O. M. Manyakina ◽  
I. S. Akkuratova-Maksimova
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Intestinal Metaplasia ◽  
Chronic Gastritis ◽  
Young Patients ◽  
Chain Reaction ◽  
Highly Pathogenic ◽  
Genetic Characteristics ◽  
Polymerase Chain ◽  
Caga Status

Objective. To evaluate the effect of the genetic characteristics of Helicobacter pylori on the nature of pathomorphological disorders in the gastric mucosa in chronic Hp-associated gastritis in young people. Material and methods. Forty-two adults (25 men and 17 women) aged 19 to 40 years with Hp-associated chronic gastritis were examined. The severity and activity of inflammation, as well as the presence of atrophy and intestinal metaplasia were determined in gastrobioptates. Genetic typing of Hp was performed for 16 pathogenicity factors of infect: CagA, CagM, CagT, CagH, CagC, CagF, CagE, VacAs1 and As2, IceA, Baba; HpaA; OipA, AlpB; UreB and UreI using polymerase chain reaction. Results. Pathogenic Hp strains were detected in 59.5 % of patients. Factors of adhesion HpaA (83.3 %), OipA (81 %), and AlpB (83.3 %) were identified with the highest frequency. In 57.1 % of cases, cytotoxin of the Cag group was detected, and 54.8 % of patients had a positive CagA-status. The VacA S1 allele was registered in 73.8 %, VacA S2 in 4.8 %, IceA in 38.1 %, and BabA in 45.2 % of cases. The presence of Hp strains in the gastric mucosa, which have three or more pathogenicity island genes, significantly increases the severity and activity of the inflammatory process, revealing signs of moderate atrophy of the digestive tract and intestinal metaplasia. Conclusions. Colonization of the gastric mucosa in young patients with Hp-associated chronic gastritis by highly pathogenic Hp strains leads to severe violations of its morphology.

scholarly journals Genetic characterization of the helicobacter pylori infection in adolescents with chronic gastritis

2019 ◽  
pp. 27-30
Author(s):  
E. M. Spivak ◽  
O. M. Manyakina ◽  
R. M. Levit ◽  
M. Yu. Kirillov ◽  
L. V. Ogneva ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Genetic Characterization ◽  
Clinical Manifestations ◽  
Chain Reaction ◽  
Highly Pathogenic ◽  
Genetic Characteristics ◽  
Polymerase Chain

The aim of the work. To establish the features of clinical manifestations and pathomorphology of gastric mucosa in Hp - associated chronic gastritis in adolescents, depending on the genetic characteristics of Hp. Patients and methods. In 133 adolescents with Hp-associated gastritis, polymerase chain reaction was used to determine the presence of pathogenicity factors in the HP genome. Results. In 60,9% of cases, highly pathogenic strains of Helicobacter pylori containing genes Cag (A, C, E, F, H, M, T), UreB, UreI, VacAs1, IceA, BabA, hpaA, AlpB and OipA are detected. Conclusion. The presence of highly pathogenic strains of Hp does not affect the clinical manifestations of gastritis, but is associated with high rates of contamination, increased inflammation, the appearance of signs of atrophy of the gastric mucosa.

scholarly journals Helicobacter pylori and Epstein–Barr Virus Infection in Gastric Diseases: Correlation with IL-10 and IL1RN Polymorphism

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Fasciana Teresa ◽  
Nicola Serra ◽  
Giuseppina Capra ◽  
Chiara Mascarella ◽  
Cesare Gagliardi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Epstein Barr Virus ◽  
Normal Gastric Mucosa ◽  
Gastric Diseases ◽  
Barr Virus ◽  
Genes Encoding ◽  
Epstein Barr

Introduction. Helicobacter pylori and Epstein–Barr virus (EBV) infection have recently been shown to be associated with gastric diseases. Polymorphisms in genes encoding cytokines such as interleukin 10 (IL-10) and interleukin 1 Receptor (IL-1RN) influence cytokine secretion levels and appear to contribute to the risk of developing gastroduodenal diseases. To our knowledge, this is the first preliminary study to address the association of coinfection with H. pylori and EBV and their correlation with genetic predisposition in the development of gastric diseases. Methods. Gastric biopsy samples of 96 patients with different gastric diseases were used. Results. Our results showed that the rate of coinfection was higher in patients with gastric cancer than in patients with normal gastric mucosa, active chronic gastritis, and MALT lymphoma. As regards the characterization of H. pilory strains, the polymorphism s1m1i1 of vacA gene was more frequent in patients with MALT Lymphoma in comparison to others, while the polymorphism s2m2i2 was most frequent in patients with normal gastric mucosa. In addition, patients who tested positive for the cagA gene were more frequently those affected with gastric cancer than those with inactive chronic gastritis. Similarly, the patients with oipA gene ON were more frequently those with gastric cancer than those with inactive chronic gastritis. Conclusion. According to our analysis, there was no correlation between coinfection and polymorphisms in genes encoding IL-10 and IL-1RN. We conclude that various factors can be involved in the development of gastric diseases.

scholarly journals The Role of Gastric Mucosal Immunity in Gastric Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Siru Nie ◽  
Yuan Yuan
Keyword(s):  
Gastric Mucosa ◽  
Immune Responses ◽  
Mucosal Immunity ◽  
Basic Feature ◽  
Gastric Diseases ◽  
Innate And Adaptive Immunity ◽  
Barr Virus ◽  
Epstein Barr ◽  
Disease Understanding

Gastric mucosa plays its immune function through innate and adaptive immunity by recruiting immune cells and releasing corresponding cytokines, which have an inseparable relationship with gastric diseases. Whether infective gastric diseases caused by Helicobacter pylori, Epstein-Barr virus or other microbe, noninfective gastric diseases, or gastric cancer, gastric mucosal immunity plays an important role in the occurrence and development of the disease. Understanding the unique immune-related tissue structure of the gastric mucosa and its role in immune responses can help prevent gastric diseases or treat them through immunotherapy. In this review, we summarize the basic feature of gastric mucosal immunity and its relationship with gastric diseases to track the latest progress of gastric mucosal immunity, update relevant knowledge and provide theoretical reference for the prevention and treatment of gastric diseases based on the gastric mucosal immunity.

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.

scholarly journals The prognosis of chronic erosive gastritis associated with Helicobacter pylori and Epstein-Barr

2019 ◽  
pp. 61-64
Author(s):  
T. E. Afanasenkova ◽  
E. E. Dubskaya ◽  
S. M. Bazhenov
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Epstein Barr Virus ◽  
Erosive Gastritis ◽  
Barr Virus ◽  
Presence And Absence ◽  
Epstein Barr

Аim. To study the severity of chronic erosive gastritis associated with Helicobacter pylori and Epstein-Barr virus depending on the number of copies of Epstein-Barr virus in biopsies of gastric mucosa. Materials and methods. The severity of chronic erosive gastritis associated with Helicobacter pylori in the presence and absence of Epstein-Barr virus in the gastric mucosa was compared in 65 patients, divided into 4 groups depending on the detection of Epstein-Barr virus in the gastric mucosa. Result. the presence of Epstein-Barr virus in the gastric mucosa aggravates the course of chronic erosive gastritis associated with Helicobacter pylori.

scholarly journals Peculiarities of humoral immunity against Epstein-Barr virus and Helicobacter pylori of gastric mucosa in patients with stomach dysplasia and cancer

2017 ◽  
Vol 94 (11) ◽  
pp. 832-836
Author(s):  
Marina V. Vusik ◽  
R. I. Pleshko ◽  
T. V. Avdeenko ◽  
O. V. Cheremisina ◽  
O. A. Matveenko
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Humoral Immunity ◽  
Epstein Barr Virus ◽  
Neoplastic Tissue ◽  
Barr Virus ◽  
High Prevalence ◽  
Low Levels ◽  
Epstein Barr ◽  
High Level

High prevalence of infection with Epstein-Barr virus (EBV) andpotentially oncogenic Helicobacter pylori requires understanding their role in pre-cancerous and cancerous processes. We studied peculiarities of humoral immunity against Epstein-Barr virus and the severity of viral infestation in patients with stomach dysplasia, cancer and concomitant infection of gastric mucosa with H.pylori. It was shown that the development of dysplastic changes in the infected mucosa is most frequently associated with high titers of IgG and IgA to capsid antigen and early EBV antigens which suggests their cooperation in the development ofprecancerous disorders. The character of antiviral humoral reactions in cancer patients depends on viral infestation of the neoplastic tissue. ECB and H.pylori infections are mutually exclusive in such patients. The absence of H.pylori is associated with the high level of antiviral humoral reactions and high infestation of the neoplastic tissue with EBV whereas low levels of antiviral humoral reactions occur in patients with H.pylori infection.

scholarly journals Problematic issues of chronic gastritis studies

2019 ◽  
Vol 44 (3) ◽  
pp. 54-61
Author(s):  
Y. S. Tsimmerman ◽  
Yu. A. Zakharova
Keyword(s):  
Helicobacter Pylori ◽  
Chronic Gastritis ◽  
Inflammatory Process ◽  
History Of ◽  
Histological Characteristics ◽  
Functional Features ◽  
Bacterial Associations ◽  
The 19Th Century ◽  
Gastric Microflora

The article defines chronic gastritis as a polyetiological and polypathogenetic stomach disease with a chronic, slowly progressing course, which is based on a specific inflammatory process with lymphoplasmocytic infiltration of its mucosa and neutrophilic component indicating its activity, and with development of disregenerative, dystrophic changes, leading to its secretory insufficiency, manifested hypo- and achlorhydria and gastric achilia. The history of studying chronic gastritis from the beginning of the 19th century till present days is briefly described. It is proposed to distinguish between causal (Helicobacter pylori, etc.) and predisposing (alcohol, smoking, coarse food, etc.) factors in the development of chronic gastritis. The analysis of various classifications of gastritis is carried out: based on etiology, pathogenesis, functional features, clinic, endoscopic and histological characteristics. The Sydney, Houston classifications, the OLGA system are described. Particular attention is paid to diagnosis, biopsy technique of the gastric mucosa, ratio of diagnoses of chronic gastritis and functional dyspepsia, as well as the role of gastric microflora in development of gastritis. It is revealed that gastric microflora in chronic gastritis is represented by numerous types of bacteria (more often in the form of bacterial associations), moreover, Helicobacter pylori is not the dominant microorganism colonizing the stomach, and the mucosal microflora found in the stomach has adhesiveness, invasiveness and pathogenic properties, including its urease activity.

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