Tissue transglutaminase activity in human gastric mucosa according to Helicobacter pylori infection

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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Disappearance of Helicobacter without Antibiotics in 12 Patients with Gastritis

Canadian Journal of Gastroenterology ◽

10.1155/1997/423496 ◽

1997 ◽

Vol 11 (2) ◽

pp. 167-172 ◽

Cited By ~ 6

Author(s):

Hugh James Freeman

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Natural History ◽

Gastric Biopsy ◽

Endoscopic Procedures ◽

History Of ◽

Gastric Biopsies ◽

H Pylori ◽

Upper Gastrointestinal

Detection ofHelicobacter pyloriin endoscopic gastric biopsies has been associated with a variety of diseases, including ulcers and gastritis. Although the natural history ofH pyloriin the gastric mucosa is unknown, antibiotic regimens have been used for eradication. Gastric biopsies from 6050 endoscopic procedures done by a single gastroenterologist from 1981 to 1994 were evaluated. Of these, 2860 from April 1, 1991 to September 30, 1994 had silver-stained biopsies to facilitateH pyloridetection, and at least two upper endoscopic procedures were done with gastric biopsies in 188 patients. Twelve of the 188 patients with an initially positiveH pylorigastric biopsy becameH pylori-negative without antibiotic treatment forH pylorior other infection; 10 received omeprazole and two received no drug treatment. In two of the 12 patients recurrentH pyloriin the gastric mucosa was also documented. These findings indicate thatH pylorimay disappear and reappear in the gastric mucosa with no specific antibiotic eradication regimen, although omeprazole may eradicateH pyloriin vivo in some patients. The natural history ofH pyloriin gastric biopsies is poorly understood. Improved understanding, especially regarding the pathogenesis of upper gastrointestinal ulcerative and inflammatory disease processes, is essential before recommendations for specific antibiotic eradication regimens can be made.

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

The Journal of Immunology ◽

10.4049/jimmunol.172.12.7734 ◽

2004 ◽

Vol 172 (12) ◽

pp. 7734-7743 ◽

Cited By ~ 41

Author(s):

Amato de Paulis ◽

Nella Prevete ◽

Isabella Fiorentino ◽

Andrew F. Walls ◽

Monica Curto ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Helicobacter Pylori Infection ◽

Human Gastric Mucosa ◽

H Pylori

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Natural history of helicobacter pylori infection from infancy to adulthood: A 21-year follow-up cohort study

Gastroenterology ◽

10.1016/s0016-5085(01)80628-4 ◽

2001 ◽

Vol 120 (5) ◽

pp. A128-A128 ◽

Cited By ~ 1

Author(s):

H MALATY ◽

D GRAHAM ◽

A ELKASABANY ◽

S REDDY ◽

S SRINIVASAN ◽

...

Keyword(s):

Helicobacter Pylori ◽

Cohort Study ◽

Natural History ◽

Helicobacter Pylori Infection ◽

History Of

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P.06.10 NATURAL HISTORY OF GASTRIC ULCER IN A 25 YEARS FOLLOW-UP: ROLE OF HELICOBACTER PYLORI INFECTION AND NONSTEROIDAL ANTI-INFLAMMATORY DRUGS

Digestive and Liver Disease ◽

10.1016/s1590-8658(18)30530-9 ◽

2018 ◽

Vol 50 (2) ◽

pp. e182-e183

Author(s):

C. Miraglia ◽

O. Cavatorta ◽

L. Franzoni ◽

P. Crafa ◽

N. Dal Bo' ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Ulcer ◽

Natural History ◽

Helicobacter Pylori Infection ◽

History Of ◽

Inflammatory Drugs ◽

Anti Inflammatory

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Helicobacter pylori infection is associated to increased levels of tissue transglutaminase in gastric mucosa cells

Gastroenterology ◽

10.1016/s0016-5085(08)83332-x ◽

2001 ◽

Vol 120 (5) ◽

pp. A670 ◽

Cited By ~ 1

Author(s):

Maria P. Dore ◽

Anna F. Naitana ◽

Yoshio Yamaoka ◽

Silvana Sanna ◽

Rita Mele ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Tissue Transglutaminase ◽

Helicobacter Pylori Infection

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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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