Analysis of Helicobacter pylori vacA andcagA genotypes and serum antibody profile in benign and malignant gastroduodenal diseases

Background—Helicobacter pylori species comprise different strains, cytotoxic and non-cytotoxic, which can be identified on the basis of their genomic pattern.Aims—(1) To evaluate the polymorphism of the vacA gene and to ascertain whether thecagA gene is present in patients with gastric adenocarcinoma. (2) To study the anti-H pylori antibody profile using western blotting.Patients—Twenty one patients with gastric adenocarcinoma and 71 with H pyloriassociated benign disease (nine gastric ulcer, 29 duodenal ulcer, 25 antral gastritis, and eight duodenitis).Methods—The polymerase chain reaction was used to verify the presence or absence ofcagA and to study the polymorphism of vacA in gastric mucosal samples obtained during endoscopy for patients with benign diseases and at surgery for patients with gastric adenocarcinoma. Fasting sera were used to assess anti-H pylori antibodies against different H pyloriantigens by western blotting.Results—cagAgene and the allele s1 of vacAwere significantly less frequent in patients with antral gastritis (60% and 60%) compared with patients with gastric adenocarcinoma (94% and 100%) and with other non-malignant gastroduodenal diseases (93% and 87%) (χ2=16.01, p<0.001; and χ2=13.97, p<0.01). In patients with gastric adenocarcinoma, antibodies against a 74 kDa H pylori antigen were less frequently found than in patients with benign diseases.Conclusions—H pylori infection caused bycagApositive/vacA s1 strains is a frequent finding in patients with gastric adenocarcinoma. Prospective studies are needed to confirm whether the low incidence of positive serological response to the 74 kDa H pyloriantigen in patients with gastric adenocarcinoma is important.

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Serum Antibody Responses to Helicobacter pylori and the cagA Marker in Patients with Mucosa-Associated Lymphoid Tissue Lymphoma

Clinical and Diagnostic Laboratory Immunology ◽

10.1128/cdli.6.4.633-638.1999 ◽

1999 ◽

Vol 6 (4) ◽

pp. 633-638 ◽

Cited By ~ 8

Author(s):

Anne Taupin ◽

Alessandra Occhialini ◽

Agnès Ruskone-Fourmestraux ◽

Jean-Charles Delchier ◽

Jean-Claude Rambaud ◽

...

Keyword(s):

Helicobacter Pylori ◽

Antibody Response ◽

Malt Lymphoma ◽

Lymphoid Tissue ◽

Serum Antibody ◽

Dot Blot ◽

Homologous Strain ◽

H Pylori ◽

Different Strains ◽

Dot Blot Analysis

ABSTRACT The lymphoma of the mucosa-associated lymphoid tissue (MALT) of the stomach has been linked to Helicobacter pylori infection, but the mechanisms involved in B-cell proliferation remain elusive. In a search for putative H. pylori-specific monoclonal immunoglobulin production, an H. pylori strain was isolated from 10 patients with MALT lymphoma and used to detect the specific serum antibody response to the homologous strain by immunoblotting. Moreover, the antigenicity of the different strains was compared by using each of the 10 sera. We found that the different strains induced highly variable patterns of systemic immunoglobulin G antibody response, although several bacterial antigens, such as the 60-kDa urease B, were often recognized by the different sera. ThecagA marker was detected in the strains by PCR with specific primers and by dot blot analysis, and the CagA protein was found in the sera of 4 of the 10 patients by immunoblotting. In conclusion, MALT lymphoma patients, like other patients with H. pylori gastritis, exhibit a polymorphic systemic antibody response, despite an apparently similar antigenic profile. The CagA marker of pathogenicity is not associated with this disease.

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Western Blotting of Total Lysate of Helicobacter pylori in Cases of Atrophic Body Gastritis

Clinical Chemistry ◽

10.1373/clinchem.2005.054627 ◽

2006 ◽

Vol 52 (2) ◽

pp. 220-226 ◽

Cited By ~ 12

Author(s):

Roberta Mini ◽

Bruno Annibale ◽

Edith Lahner ◽

Giulia Bernardini ◽

Natale Figura ◽

...

Keyword(s):

Helicobacter Pylori ◽

Western Blotting ◽

Chronic Atrophic Gastritis ◽

Bacterial Protein ◽

Previous Infection ◽

Multistep Process ◽

H Pylori ◽

Different Strains ◽

Diagnostic Reagent ◽

Total Lysate

Abstract Background: Atrophic body gastritis is considered the first important step in the histogenesis of gastric carcinoma, a multistep process starting from chronic gastritis and progressing through chronic atrophic gastritis, intestinal metaplasia, and dysplasia. Helicobacter pylori is involved in the induction of atrophic body gastritis, but documentation of H. pylori infection is difficult because of the progressive disappearance of the bacterium. Our study aimed to detect past H. pylori infection in patients with atrophic body gastritis. Methods: We used Western blot analyses of whole bacterial protein lysate of 2 different strains to probe sera from 143 patients. All sera were analyzed by ELISA (Bio-Rad), and results of gastric histology were available for all patients. Results: Among 111 patient sera previously classified as negative for H. pylori infection by ELISA, 106 (95.5%) were positive when assayed by immunoblotting. Conclusions: Commercial diagnostic reagent sets may fail to detect H. pylori infection. Western blotting of whole bacterial protein extracts could provide the basis of a noninvasive serology tool able to assess previous infection with H. pylori in patients with atrophic body gastritis.

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Helicobacter Pylori Infection in Patients with Gastric Adenocarcinoma

Tumori Journal ◽

10.1177/030089169608200108 ◽

1996 ◽

Vol 82 (1) ◽

pp. 40-44

Author(s):

Chew-Wun Wu ◽

Tzee-Chung Wu ◽

Yun-Ray Chang ◽

Shyh-Haw Tsay ◽

Shih-Jiun Yin ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Adenocarcinoma ◽

Serum Antibody ◽

Multivariate Logistic Regression Analysis ◽

Enzyme Linked Immunosorbent Assay ◽

Serum Samples ◽

Clinicopathologic Parameters ◽

The Difference ◽

H Pylori ◽

Infiltrative Tumor

We examined the biologic tumor behavior in Helicobacter pylori-seropositive patients with gastric adenocarcinoma. A total of 214 consecutive patients with pathologically confirmed adenocarcinoma of the stomach who underwent gastric resection were studied. The stored serum samples were tested for serum antibody to H. pylori by using a highly sensitive and specific IgG enzyme-linked immunosorbent assay. The difference in H. pylori-seropositive and seronegative patients with gastric adenocarcinoma was evaluated in terms of various clinicopathologic parameters. A multivariate logistic regression analysis was used to adjust for potential confounding variables. Antibodies to H. pylori were detected in 65.9% of patients with gastric adenocarcinoma. H. pylori-seropositive patients were younger than seronegative patients and had infiltrative tumor according to Ming's criteria. When adjusted for age, infiltrative tumor come out stronger. These findings suggest that H. pylori infection may be related to infiltrative type gastric adenocarcinoma; further study is necessary.

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Serodiagnosis and Bacterial Genome of Helicobacter pylori Infection

Toxins ◽

10.3390/toxins13070467 ◽

2021 ◽

Vol 13 (7) ◽

pp. 467

Author(s):

Aina Ichihara ◽

Hinako Ojima ◽

Kazuyoshi Gotoh ◽

Osamu Matsushita ◽

Susumu Take ◽

...

Keyword(s):

Helicobacter Pylori ◽

Antibody Titer ◽

Bacterial Genome ◽

Serum Antibody ◽

Gene Mutations ◽

Bacterial Genomes ◽

Western Blots ◽

A Genome ◽

Vaca Gene ◽

H Pylori

The infection caused by Helicobacter pylori is associated with several diseases, including gastric cancer. Several methods for the diagnosis of H. pylori infection exist, including endoscopy, the urea breath test, and the fecal antigen test, which is the serum antibody titer test that is often used since it is a simple and highly sensitive test. In this context, this study aims to find the association between different antibody reactivities and the organization of bacterial genomes. Next-generation sequences were performed to determine the genome sequences of four strains of antigens with different reactivity. The search was performed on the common genes, with the homology analysis conducted using a genome ring and dot plot analysis. The two antigens of the highly reactive strains showed a high gene homology, and Western blots for CagA and VacA also showed high expression levels of proteins. In the poorly responsive antigen strains, it was found that the inversion occurred around the vacA gene in the genome. The structure of bacterial genomes might contribute to the poor reactivity exhibited by the antibodies of patients. In the future, an accurate serodiagnosis could be performed by using a strain with few gene mutations of the antigen used for the antibody titer test of H. pylori.

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Helicobacter Pylori Induce Gastric Upset

Journal of Medical Research and Surgery ◽

10.52916/jmrs214055 ◽

2021 ◽

pp. 1-1

Author(s):

Hazim Abdul Rahman Alhit

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Serum Antibody ◽

Endoscopic Biopsy ◽

Helicobacter Pylori Infection ◽

Gastric Epithelium ◽

Gastric Diseases ◽

Heterogeneous Distribution ◽

Cytotoxin Associated Gene A ◽

H Pylori

Editorial: Helicobacter pylori is a micro-aerophilic, helical-form gramnegative aggressive bacteria. Accordingly, the idiom “Helico” intimates its helical appearance, “bacter” symbolizes bacteria, while “pylori” denotes stomach due to the first and common site of this bacteria living. Further, Marshall B. and Warren R. observed and described it in 1982. Then, the followed investigators studied this bacterium in detail with its consequences and complexities [1]. Gastric upset (Indigestion), dyspepsia: means impaired gastric digestion. Accordingly, the patient complains of upper abdominal pain, heartburn, belching, nausea, even feeling earlier gastric fullness than expected while eating. Furthermore, there are many causes of indigestion like gastroesophageal reflux disease, ulcer disease, gastritis, and even gastric cancer. Hence, unexplained recent onset dyspepsia in older people may need additional examinations. Moreover, one of the common causes is Helicobacter pylori infection, which needs laboratory and endoscopic examination [2]. Argument Many theories investigated the etiology and pathogenesis of Helicobacter pylori infection, concerning chronic or acute gastritis. Hence, gastric upset is the main presentation of both types of gastritis. Evidences The genotype is valuable in determining the dominant Helicobacter pylori strains as the isolates were different genetically plus heterogeneous distribution. Accordingly, the vac and cag markers operate a significant function in defining clinical consequences. These virulence agents are present in a subset of Helicobacter pylori strains isolates like cagA, iceA, vacA, and ureC. Moreover, the cagA causes cytotoxins induction by the gastric epithelial cell as Interleukin 8 [3]. The molecular intercommunication researches exhibit that the act of acarus calamus in hindering biofilm formation in Helicobacter pylori is due to the inhibitory impact of phytobio-active component, β-sitosterol, on the quorum sensing molecules-ToxB, PhnB, DnaA, plus Sip. Consequently, this opinion may suggest the molecular mechanism of Helicobacter pylori in producing the acidrelated complaints and gives a clue to a new therapy [4]. Helicobacter pylori infection causes lncRNA risk impression linked to H. pylori in gastric cancer patients and can prognosticate the prediction of these patients [5]. There was a close relationship between raised serum IgE levels in Helicobacter pylori infected patients [6]. Counterargument The laboratory investigations of Helicobacter pylori infection depend on several factors like the fluctuations of serum antibody titers in a time series, the antigene detection in stool tests, the false-positive results of lab tests, or the manner of endoscopic biopsy collection. Furthermore, other factors like the variations in Cytotoxin-Associated Gene A (CagA) in East Asian patients. Moreover, the gastric nodularity or atrophy, the patient’s age, the severity of the gastric mucosal infection are causes of variations in Helicobacter pylori detection at the time of the investigation [7]. Refutation The significant markers of H. pylori, the presence of the vacuolating cytotoxin (vacA), the cytotoxin-associated gene A (cagA), which induced by the direct communication with gastric epithelium factor antigen (iceA gene), and the presence of urease C gene (ureC). Consequently, all these factors play the principal factors in deciding the gastric consequences of Helicobacter infections. Conclusion Helicobacter pylori induce gastric upset by several mechanisms to form numerous Gastric diseases.

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Detection of Antibody againstHelicobacter pyloriin the Saliva of Patients with Dyspepsia

Canadian Journal of Gastroenterology ◽

10.1155/1994/628376 ◽

1994 ◽

Vol 8 (7) ◽

pp. 408-412 ◽

Cited By ~ 3

Author(s):

Robert L Clancy ◽

Allan W Cripps ◽

Diana C Taylor ◽

Lois A McShane ◽

Victor J Webster

Keyword(s):

Helicobacter Pylori ◽

Predictive Value ◽

Serum Antibody ◽

Eradication Therapy ◽

Elisa Assay ◽

Local Production ◽

Clinical Value ◽

Gut Mucosa ◽

H Pylori ◽

Serum Elisa

There is a need to develop noninvasive assays to detectHelicobacter pyloriinfection in the gastric mucosa, Current dogma predicts that the presence of antibody within saliva should accurately reflect contemporary colonization of the gut mucosa. This study examined the clinical value of a saliva enzyme-linked immunoadsorbent assay (ELISA) for anti-H pyloriantibody, compared with the serum ELISA assay, and found the sensitivity of the saliva assay was 89%, specificity 94%, accuracy 93%, positive predictive value 89% and negative predictive value 94%. Assessment following eradication therapy demonstrated that salivary antibody was a more sensitive indicator of colonization than was serum antibody. The immunoglobulin G antibody in saliva correlated best with colonization, and regression analysis was most consistent with a local production of antibody. These results indicate that detection of antibody in saliva contributes to diagnosis and management ofH pyloriinfection.

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Verrucous antral gastritis in relation to Helicobacter pylori infection, nutrition, and gastric atrophy

Gastroenterology Report ◽

10.1093/gastro/goz057 ◽

2019 ◽

Vol 8 (4) ◽

pp. 293-298

Author(s):

Naoko Tsuji ◽

Yasuko Umehara ◽

Mamoru Takenaka ◽

Yasunori Minami ◽

Tomohiro Watanabe ◽

...

Keyword(s):

Helicobacter Pylori ◽

Reflux Esophagitis ◽

English Literature ◽

Indigo Carmine ◽

Gastric Atrophy ◽

Helicobacter Pylori Infection ◽

Antral Gastritis ◽

Numerous Type ◽

History Of ◽

H Pylori

Abstract Background There have been few studies in the English literature regarding verrucous gastritis (VG). The present study investigated the clinical and endoscopic features of verrucous antral gastritis, especially focusing on Helicobacter pylori infection, nutrition, and gastric atrophy. Methods We performed a retrospective study of patients who underwent routine endoscopy with indigo carmine chromoendoscopy and a comparative study was conducted between VG-positive and VG-negative groups. VG was subdivided into classical and numerous types based on the number and distribution of verrucous lesions. Demographic, clinical, and endoscopic data including body mass index (BMI), serum albumin and cholesterol, gastric atrophy, reflux oesophagitis, Barrett’s oesophagus, and H. pylori status were collected. Univariate and multivariable analyses were performed to identify factors associated with VG. Results We analysed the data of 621 patients undergoing routine endoscopy and found that VG (n = 352) was significantly associated with increased BMI (1.12 [1.05–1.18], P < 0.01), reflux esophagitis (1.96 [1.10–3.28], P < 0.01), and H. pylori negativity with or without a history of eradication (9.94 [6.00–16.47] and 6.12 [3.51–10.68], P < 0.001, respectively). Numerous-type (n = 163) VG was associated with both closed- and open-type gastric atrophy (9.9 [4.04–21.37] and 8.10 [3.41–19.24], P < 0.001, respectively). There were no statistical differences between groups regarding age, sex, total cholesterol, albumin, and bile-colored gastric juice. Conclusions Verrucous antral gastritis was related to increased BMI, reflux esophagitis, and H. pylori negativity. Numerous-type verrucous lesions were associated with gastric atrophy. These indicate that VG may be a physiological phenomenon due to high gastric acidity, mechanical overload, and vulnerability of background mucosa.

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Immunoglobulin G Antibody against Helicobacter pylori: Clinical Implications of Levels Found in Serum

Clinical and Vaccine Immunology ◽

10.1128/cdli.9.5.1044-1048.2002 ◽

2002 ◽

Vol 9 (5) ◽

pp. 1044-1048 ◽

Cited By ~ 2

Author(s):

Tseng-Shing Chen ◽

Fen-Yau Li ◽

Full-Young Chang ◽

Shou-Dong Lee

Keyword(s):

Helicobacter Pylori ◽

Chronic Gastritis ◽

Predictive Value ◽

Linear Regression Analysis ◽

Serum Antibody ◽

Quantitative Detection ◽

Enzyme Linked Immunosorbent Assay ◽

Multivariate Linear Regression Analysis ◽

H Pylori ◽

Antibody Levels

ABSTRACT The clinical significance of high levels of antibody against Helicobacter pylori is still unclear. We sought to evaluate whether the serum antibody levels could predict the presence of macroscopic gastroduodenal disease, to identify factors that correlate with antibody levels in a multivariate context, and to determine the predictive value of antibody levels for diagnosing H. pylori infection. The grades of gastritis and density of H. pylori colonization were scored separately using the updated Sydney system for antral and body mucosa. An enzyme-linked immunosorbent assay (ELISA) for the quantitative detection in serum of IgG antibodies to H. pylori was performed. Of the 170 dyspeptic patients, 105 (62%) had H. pylori infection. There was no difference in antibody levels among endoscopic findings of normal mucosa, chronic gastritis, and duodenal ulcer. On multivariate linear regression analysis, the status of H. pylori infection, mononuclear cell infiltration of body mucosa, and age correlated with antibody levels. The negative predictive value for antibody levels of <30 U/ml is 94%, and the positive predictive value of antibody levels of >70 U/ml is 98%. We conclude that serum antibody levels do not predict the severity of gastroduodenal diseases or the density of H. pylori colonization in H. pylori-infected dyspeptic patients. Higher levels are associated with the presence of H. pylori infection, the chronic gastritis score of the corpus, and older age. Setting a gray zone is necessary for ELISA, since the accuracy in this zone does not allow a precise determination of H. pylori status.

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Mucosal FOXP3-Expressing CD4+ CD25high Regulatory T Cells in Helicobacter pylori-Infected Patients

Infection and Immunity ◽

10.1128/iai.73.1.523-531.2005 ◽

2005 ◽

Vol 73 (1) ◽

pp. 523-531 ◽

Cited By ~ 186

Author(s):

Anna Lundgren ◽

Erika Strömberg ◽

Åsa Sjöling ◽

Catharina Lindholm ◽

Karin Enarsson ◽

...

Keyword(s):

T Cells ◽

Helicobacter Pylori ◽

Regulatory T Cells ◽

Gastric Adenocarcinoma ◽

Cytotoxic T Lymphocyte ◽

Duodenal Mucosa ◽

Peptic Ulcers ◽

Low Levels ◽

H Pylori ◽

And Function

ABSTRACT Helicobacter pylori chronically colonizes the stomach and duodenum and causes peptic ulcers or gastric adenocarcinoma in 10 to 20% of infected individuals. We hypothesize that the inability of patients to clear H. pylori infections is a consequence of active suppression of the immune response. Here we show that H. pylori-infected individuals have increased frequencies of CD4+ CD25high T cells in both the stomach and duodenal mucosa compared to uninfected controls. These cells have the phenotype of regulatory T cells, as they express FOXP3, a key gene for the development and function of regulatory T cells, as well as high levels of the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) protein. In contrast, mucosal CD4+ CD25low and CD4+ CD25− cells express little FOXP3 mRNA and low levels of the CTLA-4 protein. Mucosal CD4+ CD25high T cells are present in individuals with asymptomatic H. pylori infections as well as in duodenal ulcer patients. The frequencies of CD4+ CD25high cells are also increased in the stomachs of H. pylori-infected patients with gastric adenocarcinoma, particularly in cancer-affected tissues. These findings suggest that regulatory T cells may suppress mucosal immune responses and thereby contribute to the persistence of H. pylori infections.

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Helicobacter Pylori Associated Antral Gastritis in Peptic Ulcer Disease Patients and Normal Healthy Population of Kashmir, India

Diagnostic and Therapeutic Endoscopy ◽

10.1155/dte.4.135 ◽

1998 ◽

Vol 4 (3) ◽

pp. 135-139 ◽

Cited By ~ 2

Author(s):

Gh. Jeelani Romshoo ◽

G. M. Malik ◽

M. Youssuf Bhat ◽

Ab. Rashid rather ◽

Javaid Ahmad Basu ◽

...

Keyword(s):

Helicobacter Pylori ◽

Peptic Ulcer ◽

Gastric Ulcer ◽

Peptic Ulcer Disease ◽

Healthy Volunteers ◽

Chronic Gastritis ◽

Healthy Population ◽

Ulcer Disease ◽

Antral Gastritis ◽

H Pylori

Aim: To study the association of Helicobacter pylori infection with chronic antral gastritis in peptic ulcer disease patients and healthy population of Kashmir.Methods: 50 peptic ulcer patients (duodenal ulcer = 46, gastric ulcer = 2 and combined duodenal and gastric ulcer = 2) and 30 asymptomatic healthy volunteers were included in this study. Peptic ulcer was diagnosed on endoscopic examination. 4–6 punch biopsies were taken from gastric antrum in all the individuals and in case of gastric ulcer an additional biopsy was taken from the edge of the ulcer to exclude its malignant nature. Helicobacter pylori (H. pylori) organism was diagnosed using three different test methods, viz. Histology (using Giemsa Stain), Microbiology (Gram Stain) and Biochemistry (using one minute Endoscopy Room Test). Histological diagnosis of H. pylori was taken as the “gold standard” for the presence of H. pylori organism. Histological diagnosis of gastritis was made using Hematoxylin and Eosin Stain and the gastritis was classified as active chronic gastritis and superficial chronic gastritis.Results: Out of 30 peptic ulcer disease patients with associated antral gastritis, 27 (90%) were positive for H. pylori on histological examination (13 superficial chronic gastritis and 14 active chronic gastritis) whereas out of 8 healthy volunteers with histological evidence of chronic antral gastritis, H. pylori was observed in 7 individuals (87.50%) (4 active chronic gastritis and 3 superficial chronic gastritis).Conclusion: A highly significant association between H. pylori infection with chronic antral gastritis both in peptic ulcer disease patients and healthy volunteers of Kashmir was found in this study. Association between H. pylori infection and chronic gastritis was 90% in peptic ulcer group and 87.50% in healthy population (P<0.005).

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