Basophils Infiltrate Human Gastric Mucosa at Sites of Helicobacter pylori Infection, and Exhibit Chemotaxis in Response to H. pylori-derived Peptide Hp(2–20)

Tissue transglutaminase (t-TG) is a multifunctional protein involved in the healing of gastric erosions and ulcers in animal models. The aim of this study was to measure gastric t-TG activity in patients with dyspepsia according to Helicobacter pylori infection and cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) subtype status. Patients undergoing upper endoscopy not taking any medications were enrolled. Tissue-TG activity was determined in homogenates of antral specimens using a radiometric assay and was expressed in pmol/mg. The cagA and vacA genotypes were determined by PCR amplification using gene-specific oligoprimers. Data from 46 patients were available (17 of them were positive for H. pylori). Antral t-TG activity was significantly increased in H. pylori positive patients compared to H. pylori negative patients (6437 ± 3691 vs. 3773 ± 1530 pmol/mg; P = 0.001) according to Mann–Whitney U test. Patients with H. pylori negative gastritis had higher t-TG activity than patients with normal gastric mucosa. The specimens infected with cagA positive strains (72%) displayed greater t-TG activity than cagA negative samples (7358 ± 4318 vs. 4895 ± 1062 pmol/mg; P = 0.237). Similarly, t-TG activity was higher in H. pylori vacA s1/m1 strains vs. vacA s1/m2 (7429 vs. 5045 pmol/mg; P = 0.744), and vacA s1/m1 vs. s2/m2 (7429 vs. 4489 pmol/mg; P = 0.651) but the results were not significant. No differences were found between histology, endoscopy features and t-TG activity. These results show that t-TG activity is significantly greater in gastritis associated with H. pylori infection, suggesting that this enzyme is induced by inflammation and may have an important role in the natural history of human gastritis. Impact statement Tissue transglutaminase (t-TG) is unique among TG enzymes because of its additional role in several physiological and pathological activities, including inflammation, fibrosis, and wound healing. The presence of t-TG has previously been described in the intestine of human and animal models, yet studies on t-TG activity in human gastric mucosa are missing. Helicobacter pylori infection is the major cause of gastritis and peptic ulcers. For the first time, our results show that t-TG activity was significantly higher in antral specimens of patients with chronic active gastritis associated with H. pylori infection compared to H. pylori negative chronic gastritis and normal antral mucosa. These findings suggest that t-TG has a role in the natural history of human gastritis, which requires further investigation but may be an avenue for new therapeutic options.

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Helicobacter pylori infection can modulate the susceptibility of gastric mucosa cells to MNNG

Cellular & Molecular Biology Letters ◽

10.2478/s11658-006-0045-z ◽

2006 ◽

Vol 11 (4) ◽

Cited By ~ 6

Author(s):

Michał Arabski ◽

Paweł Kazmierczak ◽

Maria Wiśniewska-Jarosińska ◽

Zbigniew Morawiec ◽

Alina Morawiec-Bajda ◽

...

Keyword(s):

Gastric Cancer ◽

Dna Damage ◽

Helicobacter Pylori ◽

Gastric Mucosa ◽

Comet Assay ◽

Dietary Factors ◽

Helicobacter Pylori Infection ◽

Human Gastric Mucosa ◽

Alkaline Comet Assay ◽

H Pylori

AbstractThe pathogenesis of stomach cells can be associated with their susceptibility to exogenous dietary irritants, like nitrosamines such as dimethylnitrosamines (DMNA), and to the effects of non-dietary factors, including Helicobacter pylori infection. We used N-methyl-N’-nitro N-nitrosoguanidyne (MNNG) as a surrogate agent that induces a spectrum of DNA damage similar to DMNA. Using the alkaline comet assay, we showed that antioxidants — vitamins C and E, quercetin, and melatonin — reduced the genotoxic effect of MNNG in H. pylori-infected and non-infected human gastric mucosa cells (GMCs). To compare the sensitivity of the stomach and the blood, the experiment was also carried out in peripheral blood. We observed a higher level of DNA damage induced by MNNG in H. pylori-infected than in noninfected GMCs. We did not note any difference in the efficacy of the repair of the damage in either type of GMC. H. pylori infection may play an important role in the pathogenesis of GMCs, as it can modulate their susceptibility to dietary mutagens/carcinogens, thus contributing to gastric cancer.

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Polyphenols Reduce Gastritis Induced by Helicobacter pylori Infection or VacA Toxin Administration in Mice

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.01042-05 ◽

2006 ◽

Vol 50 (7) ◽

pp. 2550-2552 ◽

Cited By ~ 19

Author(s):

P. Ruggiero ◽

F. Tombola ◽

G. Rossi ◽

L. Pancotto ◽

L. Lauretti ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Peptic Ulcer ◽

Gastric Mucosa ◽

Atrophic Gastritis ◽

Helicobacter Pylori Infection ◽

Gastric Epithelium ◽

Human Gastric Mucosa ◽

H Pylori

ABSTRACT Helicobacter pylori colonizes the human gastric mucosa, causing inflammation that leads to atrophic gastritis, and it can cause peptic ulcer and gastric cancer. We show that polyphenol administration to mice experimentally infected by H. pylori or treated with VacA toxin can limit gastric epithelium damage, an effect that may be linked to VacA inhibition.

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Helicobacter pylori infection reduces the risk of gastroesophageal reflux disease

Experimental and Clinical Gastroenterology ◽

10.31146/1682-8658-ecg-193-9-96-101 ◽

2021 ◽

pp. 96-101

Author(s):

R. I. Khlynova ◽

O. M. Khromtsova ◽

R. B. Berdnikov ◽

I. B. Khlynov

Keyword(s):

Helicobacter Pylori ◽

Gastroesophageal Reflux Disease ◽

Gastric Mucosa ◽

Gastroesophageal Reflux ◽

Observational Study ◽

Reflux Disease ◽

Helicobacter Pylori Infection ◽

Cross Sectional ◽

Biopsy Specimens ◽

H Pylori

The aim is to study the effect of Helicobacter pylori infection on risk of developing gastroesophageal reflux disease. Materials and methods - cross-sectional observational study of 1007 patients with dyspepsia syndrome who underwent videoesophagogastroduodenoscopy with biopsy and histological examination of biopsy specimens of the gastric mucosa by OLGA-system. The age, gender, overweight, cigarette smoking, presence of Helicobacter pylori infection and gastritis stage were assessed. Results - the study showed a significant decrease in the incidence of gastroesophageal reflux disease in patients with positive H. Pylori status by 4% (RR 0,68; 95% CI, 0.49-0.94, p=0,041). The risk of developing gastroesophageal reflux disease significantly higher in overweight (RR 2,62; 95% CI 2,0-3,56; р<0,001) men (RR 1,76; 95% CI 1,33-2,32; р=0,0046) who smoked cigarettes (RR 3,23; 95% CI 2,45-4,24; р<0,001) and was not associated with the patient’s age and the stage of gastritis (р>0,05). Conclusion - a significant reduction in the frequency and risk of developing gastroesophageal reflux disease in patients with Helicobacter pylori infection is demonstrated.

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Helicobacter pylori (H. pylori) infection increases IL-8 and IL-6 production from human gastric mucosa

Gastroenterology ◽

10.1016/0016-5085(95)27387-5 ◽

1995 ◽

Vol 108 (4) ◽

pp. A769

Author(s):

T. Ando ◽

K. Kusugami ◽

M. Sakakibara ◽

T. Shimizu ◽

M. Shinoda ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Human Gastric Mucosa ◽

H Pylori

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Helicobacter pylori–binding nonacid glycosphingolipids in the human stomach

Journal of Biological Chemistry ◽

10.1074/jbc.ra118.004854 ◽

2018 ◽

Vol 293 (44) ◽

pp. 17248-17266 ◽

Cited By ~ 6

Author(s):

Chunsheng Jin ◽

Angela Barone ◽

Thomas Borén ◽

Susann Teneberg

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Structural Complexity ◽

Human Stomach ◽

Carbohydrate Binding ◽

Human Gastric Mucosa ◽

H Pylori ◽

Contrast Information

Helicobacter pylori has a number of well-characterized carbohydrate-binding adhesins (BabA, SabA, and LabA) that promote adhesion to the gastric mucosa. In contrast, information on the glycoconjugates present in the human stomach remains unavailable. Here, we used MS and binding of carbohydrate-recognizing ligands to characterize the glycosphingolipids of three human stomachs from individuals with different blood group phenotypes (O(Rh−)P, A(Rh+)P, and A(Rh+)p), focusing on compounds recognized by H. pylori. We observed a high degree of structural complexity, and the composition of glycosphingolipids differed among individuals with different blood groups. The type 2 chain was the dominating core chain of the complex glycosphingolipids in the human stomach, in contrast to the complex glycosphingolipids in the human small intestine, which have mainly a type 1 core. H. pylori did not bind to the O(Rh−)P stomach glycosphingolipids, whose major complex glycosphingolipids were neolactotetraosylceramide, the Lex, Lea, and H type 2 pentaosylceramides, and the Ley hexaosylceramide. Several H. pylori-binding compounds were present among the A(Rh+)P and A(Rh+)p stomach glycosphingolipids. Ligands for BabA-mediated binding of H. pylori were the Leb hexaosylceramide, the H type 1 pentaosylceramide, and the A type 1/ALeb heptaosylceramide. Additional H. pylori-binding glycosphingolipids recognized by BabA-deficient strains were lactosylceramide, lactotetraosylceramide, the x2 pentaosylceramide, and neolactohexaosylceramide. Our characterization of human gastric receptors required for H. pylori adhesion provides a basis for the development of specific compounds that inhibit the binding of this bacterium to the human gastric mucosa.

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The Exopolysaccharide of Lactobacillus fermentum UCO-979C Is Partially Involved in Its Immunomodulatory Effect and Its Ability to Improve the Resistance against Helicobacter pylori Infection

Microorganisms ◽

10.3390/microorganisms8040479 ◽

2020 ◽

Vol 8 (4) ◽

pp. 479

Author(s):

Valeria Garcia-Castillo ◽

Guillermo Marcial ◽

Leonardo Albarracín ◽

Mikado Tomokiyo ◽

Patricia Clua ◽

...

Keyword(s):

Immune Response ◽

Helicobacter Pylori ◽

Gastric Mucosa ◽

Innate Immune Response ◽

Innate Immune ◽

Helicobacter Pylori Infection ◽

Beneficial Effects ◽

Ifn Γ ◽

H Pylori

Lactobacillus fermentum UCO-979C (Lf979C) beneficially modulates the cytokine response of gastric epithelial cells and macrophages after Helicobacter pylori infection in vitro. Nevertheless, no in vivo studies were performed with this strain to confirm its beneficial immunomodulatory effects. This work evaluated whether Lf979C improves protection against H. pylori infection in mice by modulating the innate immune response. In addition, we evaluated whether its exopolysaccharide (EPS) was involved in its beneficial effects. Lf979C significantly reduced TNF-α, IL-8, and MCP-1 and augmented IFN-γ and IL-10 in the gastric mucosa of H. pylori-infected mice. The differential cytokine profile induced by Lf979C in H. pylori-infected mice correlated with an improved reduction in the pathogen gastric colonization and protection against inflammatory damage. The purified EPS of Lf979C reduced IL-8 and enhanced IL-10 levels in the gastric mucosa of infected mice, while no effect was observed for IFN-γ. This work demonstrates for the first time the in vivo ability of Lf979C to increase resistance against H. pylori infection by modulating the gastric innate immune response. In addition, we advanced knowledge of the mechanisms involved in the beneficial effects of Lf979C by demonstrating that its EPS is partially responsible for its immunomodulatory effect.

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Protease-Activated Receptor-2 (PAR2) in Human Gastric Mucosa as Mediator of Proinflammatory Effects in Helicobacter pylori Infection

Helicobacter ◽

10.1111/j.1523-5378.2011.00866.x ◽

2011 ◽

Vol 16 (6) ◽

pp. 452-458 ◽

Cited By ~ 4

Author(s):

Arne Kandulski ◽

Doerthe Kuester ◽

Klaus Mönkemüller ◽

Lucia Fry ◽

Peter Malfertheiner ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Helicobacter Pylori Infection ◽

Human Gastric Mucosa ◽

Protease Activated Receptor 2

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Lipids of human gastric mucosa: Effect of Helicobacter pylori infection and nonalcoholic cirrhosis

Gastroenterology ◽

10.1016/0016-5085(94)90160-0 ◽

1994 ◽

Vol 107 (2) ◽

pp. 362-368 ◽

Cited By ~ 22

Author(s):

Gerardo Nardone ◽

Francesco D'Armiento ◽

Gaetano Corso ◽

Paolo Coscione ◽

Mauro Esposito ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Helicobacter Pylori Infection ◽

Human Gastric Mucosa

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Follow-up analysis and histopathological study of gastric mucosa in patients with Helicobacter pylori infection

Journal of International Medical Research ◽

10.1177/03000605211055397 ◽

2021 ◽

Vol 49 (12) ◽

pp. 030006052110553

Author(s):

Guang Zhao ◽

Zhishang Zhang ◽

Baohui Li ◽

Silin Huang ◽

Wensi Li ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Intraepithelial Neoplasia ◽

Mucosal Damage ◽

Helicobacter Pylori Infection ◽

Gastric Mucosal Damage ◽

Histopathological Study ◽

Significant Difference ◽

H Pylori

Objective To investigate the histomorphological characteristics of the gastric mucosa and the prognosis in patients with Helicobacter pylori infection. Methods Progressive damage to the gastric mucosa was examined by immunohistochemistry in 2294 patients with H. pylori infection and follow-up information was analyzed. Results H. pylori initially colonized the mucus layer covered by the gastric mucosa epithelium, then selectively adhered to and destroyed the surface mucus cells causing intra-gastric and extra-gastric lesions. Gastric mucosal damage induced by H. pylori was divided into five stages according to the depth of H. pylori invasion and degree of lesion deterioration: mucilaginous, surface mucocellular, lamina propria lesion, mucosal atrophy, and intraepithelial neoplasia stages. Morphological follow-up analysis revealed no significant difference in 6-month curative effects between stage I and stage II, but significant differences were found between stages II and III, stages III and IV, and between stages IV and stage V, respectively. Conclusions This novel staging strategy may be a valuable tool for diagnosing and predicting the results of gastric mucosal damage induced by H. pylori infection.

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