scholarly journals Serum IgG antibodies against Helicobacter pylori low molecular weight antigens 50kDa, 30kDa and Urease A 26 kDa, along with vacuolating cytotoxin A are associated with the outcome of the infection

2020 ◽  
Vol 77 (4) ◽  
pp. 405-412
Author(s):  
Nebojsa Manojlovic ◽  
Ivana Tufegdzic ◽  
Elizabeta Ristanovic ◽  
Dubravko Bokonjic
Keyword(s):  
Gastric Cancer ◽  
Molecular Weight ◽  
Helicobacter Pylori ◽  
Functional Dyspepsia ◽  
Low Molecular Weight ◽  
Igg Antibodies ◽  
Vacuolating Cytotoxin ◽  
Specific Outcome ◽  
H Pylori ◽  
Topographic Distribution

Background/Aim. We designed and conducted this study due to the fact that results of the previous studies about seroreactivity to low-molecular-weight Helicobacter pylori antigens, cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA) in patients with gastric cancer and peptic ulcer were conflicting. Methods. The Western blot test was performed in 123 patients, 31 with gastric cancer, 31 with duodenal ulcer, 31 with gastric ulcer, 30 with gastritis and functional dyspepsia in order to determine IgG antibodies to H. pylori antigens (CagA, VacA, Heat shock protein 60kDa, Urease B 66 kDa, Flagellin 55kDa, 50kDa, 30 kDa, Urease A 26 kDa, 24 kDa). In this study we analyzed: seroreactivity to H. pylori antigens between group with functional dyspepsia and others; between grades of different histopathological parameters of inflammation of antral and corporal mucosa and between antrum-predominant gastritis and corpus-predominant gastritis + pangastritis groups. Results. It was shown that seropositivity to 50 kDa antigen could be used as a biomarker for functional dyspepsia, seropositivity to 30 kDa antigen for antrumpredominant gastritis and H. pylori colonization in the antrum, to UreaseA26 kDa antigen for pangastritis and corpus-predominant gastritis and degree of inflammation in the corpus. Seropositivity to VacA was the biomarker for gastric cancer and peptic ulcer taken together and inflammation of antral mucosa. Seropositivity to CagA was associated with more intensive inflammation of antral and corporal mucosa, Urease B66 kDa with inflammation of corpus mucosa, but neither of them with specific outcome of H. pylori infection and topographic distribution of gastric inflammation. Conclusion. Serum IgG antibodies to H. pylori antigens 50kDa, and VacA may represent useful biomarkers for the specific outcome of H. pylori infection, while serum antibodies to 30 kDa and UreaseA26 kDa antigens might be used as specific biomarkers for different topographic distribution of inflammation in gastric mucosa.

scholarly journals Prevalence of cagA, vacA, babA2 and iceA Genes in Helicobacter pylori Strains Isolated from Colombian Patients with Functional Dyspepsia

2012 ◽  
Vol 61 (1) ◽  
pp. 33-40 ◽  
Author(s):  
AZUCENA ARÉVALO-GALVIS ◽  
ALBA A. TRESPALACIOS-RANGEL ◽  
WILLIAM OTERO ◽  
MARCELA M. MERCADO-REYES ◽  
RAÚL A. POUTOU-PIÑALES
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Molecular Markers ◽  
High Risk ◽  
Functional Dyspepsia ◽  
Allelic Variants ◽  
High Prevalence ◽  
History Of ◽  
H Pylori ◽  
New Evidence

The clinical outcome of Helicobacter pylori infection has been particularly associated with virulence genotypes. These genotypes are useful as molecular markers in the identification of patients that are infected and at high risk for developing more severe gastric pathologies. Our main objective was to determine the prevalence of virulence genotypes cagA, vacA, iceA and babA2 of H. pylori, in patients with functional dyspepsia who are infected with the bacteria. H. pylori genotypes babA2 and cagA as well as vacA and iceA allelic variants were identified by PCR in 122 isolates resulting from 79 patients with functional dyspepsia. A high prevalence of genes cagA+ (71%), vacAs1am1 (34%), babA2 (57%) and iceA1 (87%) was found. The most frequent combined genotype found were cagA+/vacAs1am1/babA2+/iceA1 and cagA-/vacAs1am1/babA2+/iceA1, regardless of any family history of gastric cancer or MALT lymphoma. The very virulent genotype cagA+/vacAs1am1/babA2+/iceA1 prevailed in the studied patients with functional dyspepsia. Our results provide information about the prevalence of four of the more important virulent factors and constitute new evidence on the prevalence of the most virulent H. pylori genotype in patients with functional dyspepsia.

scholarly journals Production of ammonium by Helicobacter pylori mediates occludin processing and disruption of tight junctions in Caco-2 cells

Microbiology ◽  
2005 ◽  
Vol 151 (10) ◽  
pp. 3267-3276 ◽  
Author(s):  
Simon D. Lytton ◽  
Wolfgang Fischer ◽  
Wolfram Nagel ◽  
Rainer Haas ◽  
Franz X. Beck
Keyword(s):  
Molecular Weight ◽  
Helicobacter Pylori ◽  
Tight Junction ◽  
Tight Junctions ◽  
Ammonium Salts ◽  
Gastric Mucosal Damage ◽  
Soluble Form ◽  
Low Molecular Weight ◽  
Partial Recovery ◽  
H Pylori

Tight junctions, paracellular permeability barriers that define epithelial cell polarity, play an essential role in transepithelial transport, cell–cell adhesion and lymphocyte transmigration. They are also important for the maintenance of innate immune defence and intestinal antigen uptake. Ammonium () is elevated in the gastric aspirates of Helicobacter pylori-infected patients and has been implicated in the disruption of tight-junction functional integrity and the induction of gastric mucosal damage during H. pylori infection. The precise mechanism of the effect of ammonium and the molecular targets of ammonium in host tissue are not yet identified. To study the effects of ammonium on epithelial tight junctions, the human colon carcinoma cell line Caco-2 was cultured on permeable supports and the transepithelial resistance (TER) was measured at different time intervals following exposure to ammonium salts or H. pylori-derived ammonium. A biphasic response to treatment with ammonium was found. Acute exposure to ammonium salts or NH3/ derived from urea metabolism by wild-type H. pylori resulted in a 20–30 % decrease in TER. After 24 h, the NH4Cl-treated cells showed a partial recovery of TER. In contrast, the control culture, or cultures that were exposed to supernatants derived from urease-deficient H. pylori, showed no significant decrease in TER. Occludin-specific immunoblots revealed the expression of a low-molecular-weight form of occludin of 42 kDa upon NH3/ exposure. The results indicate that modulation of tight-junction function by H. pylori is ammonium-dependent and linked to the accumulation of a low-molecular-weight and detergent-soluble form of occludin.

scholarly journals Relation between Seroreactivity to Low-Molecular-Weight Helicobacter pylori-Specific Antigens and Disease Presentation

2003 ◽  
Vol 10 (6) ◽  
pp. 1025-1028 ◽  
Author(s):  
Ratha-Korn Vilaichone ◽  
Varocha Mahachai ◽  
Chomsri Kositchaiwat ◽  
David Y. Graham ◽  
Yoshio Yamaoka
Keyword(s):  
Gastric Cancer ◽  
Molecular Weight ◽  
Helicobacter Pylori ◽  
Gastric Ulcer ◽  
Clinical Outcome ◽  
Cancer Patients ◽  
Serological Test ◽  
Disease Associations ◽  
H Pylori ◽  
Gastric Cancer Patients

ABSTRACT The identification of Helicobacter pylori-strain specific factors that correlate with clinical outcome has remained elusive. We investigated possible relationships between a group of H. pylori antigens and clinical outcome and compared an immunoblot assay kit (HelicoBlot, version 2.1 [HB 2.1]; Genelabs Diagnostics) with an established serological test, the high-molecular-weight cell-associated protein test (HM-CAP). We used sera from 156 Thai patients with different disease presentations, including 43 patients with gastric cancer, 64 patients with gastric ulcer, and 49 patients with nonulcer dyspepsia (NUD). HB 2.1 was compared to HM-CAP as a diagnostic test for H. pylori infection. The seroprevalence of H. pylori was significantly higher among gastric cancer patients than among patients with NUD (93 and 67%, respectively; P < 0.01). Among the H. pylori-seropositive patients, the presence of the antibody to the 37,000-molecular-weight antigen (37K antigen) was inversely related to the presence of gastric cancer (e.g., for gastric cancer patients compared with NUD patients, odds ratio [OR] = 0.28 and 95% confidence interval [CI] = 0.1 to 0.8). The presence of antibody to the 35K antigen was higher in gastric ulcer patients than in NUD patients (OR = 11.5; 95% CI = 2.4 to 54.3). The disease associations of antibodies to the 35K and 37K antigens are consistent with the possibility that these antigens are either indirect markers for H. pylori-related diseases or have specific active or protective roles in H. pylori-related diseases.

scholarly journals Diversity of Helicobacter pylori vacA andcagA Genes and Relationship to VacA and CagA Protein Expression, Cytotoxin Production, and Associated Diseases

1998 ◽  
Vol 36 (4) ◽  
pp. 944-948 ◽  
Author(s):  
Jochen Rudi ◽  
Christof Kolb ◽  
Matthias Maiwald ◽  
Dirk Kuck ◽  
Andreas Sieg ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Peptic Ulcer ◽  
Signal Sequence ◽  
Peptic Ulcers ◽  
Virulence Determinants ◽  
Middle Region ◽  
Vacuolating Cytotoxin ◽  
Ulcer Disease ◽  
H Pylori

The vacuolating cytotoxin and the cytotoxin-associated protein, encoded by vacA and cagA, respectively, are important virulence determinants of Helicobacter pylori. Sixty-five H. pylori strains were isolated from dyspeptic patients (19 with peptic ulcer disease, 43 with chronic gastritis, and 3 with gastric cancer) and studied for differences in thevacA and cagA genes and their relationship to VacA and CagA expression, cytotoxin activity, and the clinical outcome of infection. By PCR, fifty-four (83.1%) of 65 strains had thevacA signal sequence genotype s1 and only 10 (15.4%) had the type s2. After primer modification, the vacAmiddle-region types m1 and m2 were detected in 24 (36.9%) and 41 (63.1%) strains, respectively. The combinations s1-m2 (31 [47.7%]) and s1-m1 (23 [35.4%]) occurred more frequently than s2-m2 (10 [15.4%]) (P = 0.01). No strain with the combination s2-m1 was found. All 19 patients with peptic ulcers harbored type s1 strains, in contrast to 32 (74.4%) of 43 patients with gastritis (P = 0.02). The vacA genotype s1 was associated with the presence of cagA (P < 0.0001), VacA expression (P < 0.0001), and cytotoxin activity (P = 0.003). The cagA gene was detectable in 48 (73.8%) of 65 isolates and present in 16 (84.2%) of 19 ulcer patients and 29 (67.4%) of 43 patients with gastritis (P = 0.17). The vacA genotypes of GermanH. pylori isolates are identical to those previously reported. H. pylori strains of vacA type s1 are associated with the occurrence of peptic ulceration and the presence ofcagA, cytotoxin activity, and VacA expression.

scholarly journals Statins’ Regulation of the Virulence Factors of Helicobacter pylori and the Production of ROS May Inhibit the Development of Gastric Cancer

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1293
Author(s):  
Ting-Yu Lin ◽  
Wen-Hsi Lan ◽  
Ya-Fang Chiu ◽  
Chun-Lung Feng ◽  
Cheng-Hsun Chiu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Treatment Strategies ◽  
Vacuolating Cytotoxin ◽  
Cholesterol Levels ◽  
Cytotoxin Associated Gene A ◽  
H Pylori ◽  
Cellular Components ◽  
Development Of Gastric Cancer

Conventionally, statins are used to treat high cholesterol levels. They exhibit pleiotropic effects, such as the prevention of cardiovascular disease and decreased cancer mortality. Gastric cancer (GC) is one of the most common cancers, ranking as the third leading global cause of cancer-related deaths, and is mainly attributed to chronic Helicobacter pylori infection. During their co-evolution with hosts, H. pylori has developed the ability to use the cellular components of the host to evade the immune system and multiply in intracellular niches. Certain H. pylori virulence factors, including cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA), and cholesterol-α-glucosyltransferase (CGT), have been shown to exploit host cholesterol during pathogenesis. Therefore, using statins to antagonize cholesterol synthesis might prove to be an ideal strategy for reducing the occurrence of H. pylori-related GC. This review discusses the current understanding of the interplay of H. pylori virulence factors with cholesterol and reactive oxygen species (ROS) production, which may prove to be novel therapeutic targets for the development of effective treatment strategies against H. pylori-associated GC. We also summarize the findings of several clinical studies on the association between statin therapy and the development of GC, especially in terms of cancer risk and mortality.

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 The correlation between lncRNAs and Helicobacter pylori in gastric cancer

2019 ◽  
Vol 77 (9) ◽  
Author(s):  
Narges Dastmalchi ◽  
Seyed Mahdi Banan Khojasteh ◽  
Mirsaed Miri Nargesi ◽  
Reza Safaralizadeh
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Molecular Mechanisms ◽  
Gastrointestinal Diseases ◽  
Mechanisms Of Action ◽  
Molecular Pathways ◽  
Gastric Diseases ◽  
Non Coding Rnas ◽  
H Pylori ◽  
The Relationship

ABSTRACT Helicobacter pylori infection performs a key role in gastric tumorigenesis. Long non-coding RNAs (lncRNAs) have demonstrated a great potential to be regarded as effective malignancy biomarkers for various gastrointestinal diseases including gastric cancer (GC). The present review highlights the relationship between lncRNAs and H. pylori in GC. Several studies have examined not only the involvement of lncRNAs in H. pylori-associated GC progression but also their molecular mechanisms of action. Among the pertinent studies, some have addressed the effects of H. pylori infection on modulatory networks of lncRNAs, while others have evaluated the effects of changes in the expression level of lncRNAs in H. pylori-associated gastric diseases, especially GC. The relationship between lncRNAs and H. pylori was found to be modulated by various molecular pathways.

scholarly journals Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

2021 ◽  
Vol 22 (9) ◽  
pp. 4823
Author(s):  
María Fernanda González ◽  
Paula Díaz ◽  
Alejandra Sandoval-Bórquez ◽  
Daniela Herrera ◽  
Andrew F. G. Quest
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Outer Membrane ◽  
Extracellular Vesicles ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Infected Cells ◽  
H Pylori

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

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