scholarly journals Systemic and local immune responses againstHelicobacter pylori urease in patients with chronic gastritis: distinct IgA and IgG productive sites

Gut ◽  
1998 ◽  
Vol 43 (2) ◽  
pp. 168-175 ◽  
Author(s):  
S Futagami ◽  
H Takahashi ◽  
Y Norose ◽  
M Kobayashi
Keyword(s):  
B Cells ◽  
Gastric Mucosa ◽  
Immune Responses ◽  
Atrophic Gastritis ◽  
Gastric Juice ◽  
Chronic Gastritis ◽  
Specific Antibody ◽  
Histopathological Analysis ◽  
Grade Ii ◽  
H Pylori

Background—Helicobacter pylori urease is a major target for immune responses among various bacterial components in H pyloriinfected patients.Aims—To analyse the relation between systemic and local humoral immune responses toH pylori urease and grades of chronic gastritis.Patients—Seventy five patients with chronic gastritis associated with H pyloriinfection were classified into three groups (grade I, superficial gastritis; II, atrophic gastritis, quiescent; or III, atrophic gastritis, active).Methods—Anti-H pylori urease specific antibodies in the serum, gastric juice, and biopsy specimens were determined by ELISA or western blotting analysis. The sites for H pylori urease and its specific antibody producing B lymphocytes were confirmed by immunohistochemical analysis.Results—In the sera of patients with grade I gastritis, weak IgG but relatively strong IgA responses toH pylori urease were observed; dominant strong IgG responses were detected in grade II gastritis. In grade III gastritis, significant IgG and IgA responses were obtained. A similar pattern of IgA and IgG responses was detected in gastric juice and tissue. H pylori urease specific, antibody producing B cells were not found in the gastric mucosa of patients with grade I gastritis despite the presence of such B cells in the duodenal bulb. Specific B cells were observed in the gastric mucosa of patients with grade II and III gastritis with atrophy.Conclusions—PurifiedH pylori urease, together with localisation of its specific antibody producing B cells, are useful for serological testing and histopathological analysis for determining the stage of chronic gastritis and studying the pathogenesis ofH pylori infection.

scholarly journals Chronic gastritis and Helicobacter pylori in digestive form of Chagas' disease

1993 ◽  
Vol 35 (2) ◽  
pp. 117-121 ◽  
Author(s):  
A. J. A. Barbosa ◽  
D. M. M. Queiroz ◽  
A. M. M. F. Nogueira ◽  
M. J. A. Roquette Reis ◽  
E. N. Mendes ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Chagas Disease ◽  
Chronic Gastritis ◽  
Antral Mucosa ◽  
Common Cause ◽  
Superficial Gastritis ◽  
H Pylori ◽  
Inflammatory Changes

Patients with the digestive form of Chagas'disease frequently present chronic gastritis. As the microorganism Helicobacter pylori is now accepted as the most common cause of human chronic gastritis, the present work was undertaken to verify a possible relationship between the presence of this bacterium and inflammatory changes of antral mucosa in chagasic patients. Seventeen chagasics, with megaesophagus and or megacolon were studied. Fragments from two different regions of antral mucosa were obtained by endoscopy, fixed in 4% neutral formaldehyde and embedded in paraffin. The sections were stained by haematoxylin and eosin for histology analysis, and by carbolfuchsin for H. pylori identification. H. pylori was found in 16 (94.1%) chagasic patients, all of them presenting chronic gastritis. Superficial gastritis was seen in 9 (52.9%) while atrophic gastritis was present in 8 (47.1%) patients. H. pylori was present on gastric mucosa of 8 (100%) patients with atrophic gastritis and of 8 (88.8%) patients with superficial gastritis. We concluded that the microorganism H. pylori should be considered a possible factor connected with the etiopathogenesis of chronic superficial and atrophic gastritis frequently observed in patients with the digestive form of Chagas' disease.

scholarly journals H. pylori eradication therapy: impact of gastric mucosa atrophy on transport of amoxicillin to H. pylori colonization area

2021 ◽  
Vol 13 (2) ◽  
pp. 57-66
Author(s):  
Anastasiya O. Sablina ◽  
Oleg A. Sablin ◽  
Julia V. Andreeva ◽  
Gennadii G. Rodionov ◽  
I. I. Shantyr ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Gastric Juice ◽  
Eradication Therapy ◽  
Oral Drug ◽  
Antral Mucosa ◽  
Drug Infusion ◽  
Gastric Lumen ◽  
H Pylori ◽  
Systemic Transport

AIM: The aim was to assess systemic transport of amoxicillin, the most common antibiotic in H. pylori eradication regimens to the gastric in atrophic gastritis. MATERIALS AND METHODS: Systemic transport of amoxicillin to the gastric lumen of rats was evaluated in washes from the gastric mucosa in the model of atrophic gastritis after intravenous drug infusion. Transport of amoxicillin from bloodstream to the gastric lumen was also assessed in patients with atrophic and non-atrophic gastritis in aspirated via nasogastric probe gastric juice after oral drug administration. Amoxicillin concentration was measured in samples using liquid chromatography-mass spectrometry. RESULTS: In rats with induced atrophic gastritis, hyperemia and acute erosions of the gastric mucosa, as well as microscopic signs of non-active chronic body gastritis and non-active antral atrophic gastritis were found. Amoxicillin concentration in washes from the gastric mucosa was significantly (p 0.01) higher in rats of experimental group than in control group at all time points (30, 60, 120, 240 min after drug infusion). The lowest mean amoxicillin concentration in gastric juice was observed in patients with antral atrophy (p 0.01). The maximum amoxicillin concentration in gastric secretion was found at the 180th min of aspiration in patients with atrophy of gastric mucosa, while in patients of the group of comparison it was found at 30-120th min of aspiration. CONCLUSIONS: Acute gastric mucosa erosions enhance amoxicillin delivery to gastric lumen in rats. Atrophy of antral mucosa more than in the corpus is characterized by decreased amoxicillin transfer from systemic bloodstream to gastric lumen in patients after oral amoxicillin intake. The gastric mucosa atrophy should be taken into consideration while predicting the efficacy of H. pylori eradication therapy in patients with chronic gastritis.

scholarly journals Gastric Polyps and Atrophic Gastritis

2021 ◽  
Vol 31 (2) ◽  
pp. 27-33
Author(s):  
I. Yu. Kolesnikova ◽  
A. S. Novikova
Keyword(s):  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Chronic Gastritis ◽  
Eradication Therapy ◽  
Chronic Atrophic Gastritis ◽  
Low Grade ◽  
Pepsinogen I ◽  
Gastric Polyps ◽  
Critical Measure ◽  
H Pylori

Aim. A study of atrophic gastritis severity and rate in patients with gastric polyps (GP).Materials and methods. The study enrolled 61 patients with hyperplastic (HGP) and 41 — with adenomatous GP (AGP). All patients had 24-h gastric pH-metry, control of the pepsinogen I, II and gastrin-17 levels, in addition to a general clinical, endoscopic, histological examination and testing for Helicobacter pylori.Results. GP patients had benign manifestations prevailed with epigastric heaviness and overflow, and a scarce history of H. pylori testing at no control of rendered eradication therapy. A symptomatic proton pump inhibitor treatment in GP was either prescribed or voluntary. Focal atrophic gastritis in endoscopy was revealed in 12 (19.7 %) HGP and 16 (39.0 %) AGP patients, diffused atrophic gastritis — in 49 (80.3 %) HGP and 25 (60.9 %) AGP patients. Low-grade chronic gastritis in histology prevailed in HGP, moderate — in AGP, and severe — in 21.9 % cases. Moderate (27.9 %) to severe (65.6 %) atrophy of gastric mucosa was registered in HGP, with 53.7 and 39.0 % respective AGP cases. Polyp dysplasia was detected in 20 % HGP and 75.6 % AGP cases. Pepsinogen I <25 µg/L at a pepsinogen I/II ratio ><3 was observed in 38 (62.3 %) HGP and 18 (43.9 %) AGP patients. Hypo- and anacidic were 65.6 % HGP and 31.7 % AGP patients. >H. pylori-positive were 52.5 % HGP and 70.7 % AGP cases.Conclusion. A largely similar aetiopathogenesis of gastric polyps and chronic atrophic gastritis warrants the H. pylori diagnosis and a more detailed patient control for chronic gastritis grading and staging, functional insufficiency of gastric mucosa and the severity of hyperplastic and dysplastic change. The H. pylori eradication, in contrast to anti-secretory therapy, allows the containment of chronic gastritis and is a critical measure in gastric cancer prevention.

scholarly journals Statistical analysis of the сhronic gastritis in students

2020 ◽  
Vol 73 (2) ◽  
pp. 360-364
Author(s):  
Aleksandr V. Kharchenko ◽  
Nataliya V. Kharchenko ◽  
Petro M. Makarenko ◽  
Lyudmyla M. Sakharova ◽  
Pavlo V. Khomenko ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Statistical Analysis ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Mucous Membrane ◽  
Chronic Gastritis ◽  
Bacterial Contamination ◽  
The Body ◽  
Leukocyte Infiltration ◽  
Lesser Curvature

The aim: The aim of the study is a statistical analysis of the mucosa of the stomach affected by Helicobacter pylori in young people studying at the university. Materials and methods: The work contains the results of the study of chronic gastritis of type B in university volunteer students. The study was attended by students of 1-4 courses, aged 17 to 25 years, a total of 50 people. Among them were 28 men and 22 women. Results: Various forms of chronic gastritis were found in the mucosa of the topographic-anatomical sections of the stomach, 90% of which were associated with Helicobacter pylori (HP). In all departments there is a different amount of common forms of chronic gastritis. In the pyloric section only atrophic gastritis was detected – 31.0 ± 8.5. Atrophic gastritis was also dominant on the lesser curvature – 32.3 ± 7.8, but its forms were significantly (p <0.5) less pronounced than in the pyloric section. In the area of the body, the above variants of chronic gastritis were found in 34.3 ± 8.7 cases, and the majority were flat erosive gastritis 51.0 ± 9.3. There is a tendency to reduce the degree of bacterial contamination of the gastric mucosa from its pyloric section and the lesser curvature to the walls of the body. With a decrease in the degree of bacterial contamination of the gastric mucosa, the degree of leukocyte infiltration also decreases. Between the degree of contamination of the mucous membrane of Helicobacter pylori and the degree of leukocyte infiltration of the mucous membrane, the Pearson correlation coefficient is rxy – 0,935, the correlation is very strong, the coefficient of determination is D=rxy^2 – 0,874, the statistically significant dependence on the probability is 0.99. Conclusions: Atrophic or hyperplastic gastritis associated with HP is found in the gastric mucosa, respectively, 90% of cases. The degree of bacterial contamination correlates with the degree of leukocyte infiltration of the gastric mucosa. Atrophic or hyperplastic gastritis Helicobacter pylori-associated is a common disease of people in young and working age.

Urease-negative variants of H. pylori isolated from gastric mucosa of the patients with peptic ulcer and chronic gastritis

1998 ◽  
Vol 114 ◽  
pp. A1095
Author(s):  
J. Suzuki ◽  
H. Muraoka ◽  
A. Kataoka ◽  
T. Tsuchida ◽  
N. Ueda ◽  
...  
Keyword(s):  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
H Pylori

scholarly journals Escherichia coli Nissle 1917 Enhances Innate and Adaptive Immune Responses in a Ciprofloxacin-Treated Defined-Microbiota Piglet Model of Human Rotavirus Infection

mSphere ◽  
2021 ◽  
Vol 6 (2) ◽  
Author(s):  
Husheem Michael ◽  
Francine C. Paim ◽  
Stephanie N. Langel ◽  
Ayako Miyazaki ◽  
David D. Fischer ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
B Cells ◽  
Gut Microbiota ◽  
Immune Responses ◽  
Specific Antibody ◽  
T Helper ◽  
Cytotoxic Cells ◽  
Commensal Microbiota ◽  
Human Rotavirus ◽  
Enteric Infections

ABSTRACT Human rotavirus (HRV) infection is a major cause of gastroenteritis in children worldwide. Broad-spectrum antibiotic-induced intestinal microbial imbalance and the ensuing immune-metabolic dysregulation contribute to the persistence of HRV diarrhea. Escherichia coli Nissle 1917 (EcN), a Gram-negative probiotic, was shown to be a potent immunostimulant and alleviated HRV-induced diarrhea in monocolonized gnotobiotic (Gn) piglets. Our goal was to determine how EcN modulates immune responses in ciprofloxacin (Cipro)-treated Gn piglets colonized with a defined commensal microbiota (DM) and challenged with virulent HRV (VirHRV). Cipro given in therapeutic doses for a short term reduced serum and intestinal total and HRV-specific antibody titers, while EcN treatment alleviated this effect. Similarly, EcN treatment increased the numbers of total immunoglobulin-secreting cells, HRV-specific antibody-secreting cells, activated antibody-forming cells, resting/memory antibody-forming B cells, and naive antibody-forming B cells in systemic and/or intestinal tissues. Decreased levels of proinflammatory but increased levels of immunoregulatory cytokines and increased frequencies of Toll-like receptor-expressing cells were evident in the EcN-treated VirHRV-challenged group. Moreover, EcN treatment increased the frequencies of T helper and T cytotoxic cells in systemic and/or intestinal tissues pre-VirHRV challenge and the frequencies of T helper cells, T cytotoxic cells, effector T cells, and T regulatory cells in systemic and/or intestinal tissues postchallenge. Moreover, EcN treatment increased the frequencies of systemic and mucosal conventional and plasmacytoid dendritic cells, respectively, and the frequencies of systemic natural killer cells. Our findings demonstrated that Cipro use altered immune responses of DM-colonized neonatal Gn pigs, while EcN supplementation rescued these immune parameters partially or completely. IMPORTANCE Rotavirus (RV) is a primary cause of malabsorptive diarrhea in children and is associated with significant morbidity and mortality, especially in developing countries. The use of antibiotics exacerbates intestinal microbial imbalance and results in the persistence of RV-induced diarrhea. Probiotics are now being used to treat enteric infections and ulcerative colitis. We showed previously that probiotics partially protected gnotobiotic (Gn) piglets against human RV (HRV) infection and decreased the severity of diarrhea by modulating immune responses. However, the interactions between antibiotic and probiotic treatments and HRV infection in the context of an established gut microbiota are poorly understood. In this study, we developed a Gn pig model to study antibiotic-probiotic-HRV interactions in the context of a defined commensal microbiota (DM) that mimics aspects of the infant gut microbiota. Our results provide valuable information that will contribute to the treatment of antibiotic- and/or HRV-induced diarrhea and may be applicable to other enteric infections in children.

scholarly journals Chronic gastritis and precancerous diseases of the stomach: Is there a chance of a correct diagnosis?

2021 ◽  
Vol 13 (1) ◽  
pp. 85-102
Author(s):  
Aleksandr V. Tryapitsyn ◽  
Vladimir A. Malkov ◽  
Emil M. Gasanov ◽  
Ilya Belyakov
Keyword(s):  
Gastric Mucosa ◽  
Intestinal Metaplasia ◽  
Chronic Gastritis ◽  
Correct Diagnosis ◽  
Intraepithelial Neoplasia ◽  
Autoimmune Gastritis ◽  
Low Grade ◽  
Adequate Treatment ◽  
H Pylori ◽  
Almost All

AIM: The purpose of the study is to investigate the occurrence of the main forms of chronic gastritis, metaplastic and dysplastic changes in the gastric mucosa, the degree of their severity, and to assess their potential risk for the development of gastric cancer. MATERIALS AND METHODS: The study involved 2982 patients who underwent esophagogastroduodenoscopy with a standard biopsy of the gastric mucosa for morphological assessment and bacterioscopy. If autoimmune gastritis was suspected, an additional serological diagnosis was performed. When detecting intestinal metaplasia of the gastric mucosa as well as neoplastic changes according to the histological report, the description of this report was analyzed in order to identify possible equivalents in the macroscopic description of the mucous membrane. RESULTS: Out of 2982 histological studies of gastric mucosa biopsies, 1273 cases (42.7%) were found to contain H. pylori contamination. In 726 cases (24.3%), intestinal metaplasia. 66 biopsies (2.21%) showed the presence of low-grade intraepithelial neoplasia of the mucosa, 2 biopsies showed indeterminate neoplasia and 4 biopsies showed high-grade neoplasia. In 3 out of the total number of the samples, intravascular gastric adenocarcinoma was detected. In 168 cases (5.6%), gastritis was detected with predominant inflammation of the fundal region characteristic of autoimmune gastritis. In 286 biopsies (10.6%), inflammatory and/or atrophic changes and/or metaplastic changes were preserved, which, as a rule, did not have high activity and pronounced inflammation. In the remaining 1279 cases (42.9%), there was no significant inflammation or atrophic changes. The analysis of endoscopic findings showed that the detectability of intestinal metaplasia of the gastric mucosa without a biopsy study was 13.3%. DISCUSSION OF THE RESULTS: According to the results of the conducted research and analysis, it can be stated that at present, the correct diagnosis of chronic gastritis with the establishment of the etiological factor, prognosis and risks of stomach cancer development is practically not feasible within the modern health care system. This not only deprives a doctor of the opportunity to make a correct diagnosis and prescribe adequate treatment to a patient, but also makes almost all cascades of carcinogenesis, including early cancer, invisible.

scholarly journals Impact of alcohol on gastric mucosa in a population with high prevalence of Helicobacter pylori

2021 ◽  
Vol 8 (6) ◽  
pp. 764
Author(s):  
Sultan Nawahir ◽  
George Kurian ◽  
Thomas Alexander ◽  
Susy Kurian
Keyword(s):  
Gastric Mucosa ◽  
Alcohol Abuse ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Premalignant Lesions ◽  
Control Group ◽  
Chronic Alcohol ◽  
Chronic Alcohol Abuse ◽  
High Prevalence ◽  
H Pylori

Background: The purpose of the study was to see whether chronic alcohol abuse had any effect on the gastric mucosa in a population already affected by a high prevalence of Helicobacter pylori.Methods: 35 males with a history of chronic alcohol abuse were compared with 35 males who were abstinent or social drinkers. All subjects had complaints of dyspepsia. All subjects underwent endoscopy and targeted biopsies were taken from three specific sites in the stomach, namely body, antrum and incisura. Biopsies were studied to look for changes of atrophic gastritis and intestinal metaplasia. The presence or absences of H. pylori on the tissue biopsy were also recorded.Results: Atrophic gastritis were only assessable in 24 alcoholic patients and 21 non-alcoholic patients due to the inadequacy of the depth of the biopsy. AG were found to be equally distributed in both the groups. 23 (64.9%) patients in the alcoholic group and 19(54.5%) in the control group had AG (OR-1.54, p=0.47). Intestinal metaplasia was seen in 10 (28.5%) alcoholic group and 12 (34.2) in the control group (OR-0.65, p=0.45). Of the 42 subjects detected to have AG, 16 (38.1%) had IM. However, IM were always associated with AG. In addition, H. pylori were not seen to be different in the two groups. H. pylori were positive in 18 (51.4%) alcoholic and14 (40%) non-alcoholic patients (p=0.33).Conclusions: Chronic alcohol abuse doesn’t appear to have any major impact on the gastric mucosa in terms of producing premalignant lesions such as atrophic gastritis or intestinal metaplasia or enhancing the prevalence of H. pylori.

scholarly journals Production of Autoantibodies by Murine B-1a Cells Stimulated with Helicobacter pylori Urease through Toll-Like Receptor 2 Signaling

2011 ◽  
Vol 79 (12) ◽  
pp. 4791-4801 ◽  
Author(s):  
Fumiko Kobayashi ◽  
Eri Watanabe ◽  
Yohko Nakagawa ◽  
Shingo Yamanishi ◽  
Yoshihiko Norose ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
B Cells ◽  
Specific Antibody ◽  
Enzyme Linked Immunosorbent Assay ◽  
Autoantibody Production ◽  
Content Type ◽  
Murine Spleen ◽  
Neutralizing Capacity ◽  
Toll Like Receptor 2 ◽  
H Pylori

ABSTRACTHelicobacter pyloriinfection is associated with several autoimmune diseases, in which autoantibody-producing B cells must be activated. Among these B cells, CD5-positive B-1a cells from BALB/c mice were confirmed to secrete autoantibodies when cocultured with purifiedH. pyloriurease in the absence of T cells. To determine the mechanisms for autoantibody production, CD5-positive B-1a cells were sorted from murine spleen cells and stimulated with either purifiedH. pyloriurease orH. pyloricoated onto plates (referred to hereafter as plate-coatedH. pylori), and autoantibody production was measured by enzyme-linked immunosorbent assay (ELISA). Complete urease was not secreted fromH. pyloribut was visually expressed over the bacterium-like endotoxin. Urease-positive plated-coatedH. pyloristimulated B-1a cells to produce autoantibodies, although urease-deficient isotype-matchedH. pyloridid not. Autoantibody secretion by B-1a cells was inhibited when bacteria were pretreated with anti-H. pyloriurease-specific antibody having neutralizing ability against urease enzymatic activity but not with anti-H. pyloriurease-specific antibody without neutralizing capacity. The B-1a cells externally express various Toll-like receptors (TLRs): TLR1, TLR2, TLR4, and TLR6. Among the TLRs, blocking of TLR2 on B-1a cells with a specific monoclonal antibody (MAb), T2.5, inhibited autoantibody secretion when B-1a cells were stimulated with plate-coatedH. pyloriorH. pyloriurease. Moreover, B-1a cells from TLR2-knockout mice did not produce those autoantibodies. The present study provides evidence that functional urease expressed on the surface ofH. pyloriwill directly stimulate B-1a cells via innate TLR2 to produce various autoantibodies and may induce autoimmune disorders.

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