Helicobacter pylori: host responses in peptic ulceration

Xiang, Zhaoying; Bugnoli, M; Rappuoli, Rino; Covacci, Antonello; Ponzetto, Antonio; Crabtree, J. E.

doi:10.1016/0140-6736(93)93113-f

Cited by 41 publications

(15 citation statements)

References 3 publications

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“…Previous studies have shown that proliferation of T cells and macrophages is induced by cytotoxin and H. pylori, resulting in the relase of several cytokines (interleukin [IL]-2 and IL-6), which leads to the proliferation of B cells and the development of lymphoid follicles and aggregates in the infected gastric mucosa. The infiltration of T cells decreased significantly when H. pylori was eradicated or reduced in number after treatment, resulting in reduced stimulation of B cell proliferation and the disappearance of lymphoid tissue hyperplasia in the gastric mucosa (22)(23)(24)(25)(26)(27)(28). ADA is an important enzyme participating in purine and DNA metabolism.…”

Section: Discussionmentioning

confidence: 99%

Association of Adenosine Deaminase, Superoxide Dismutase, and Catalase Activities with Helicobacter pylori

et al. 2005

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Our purpose was to investigate associations between adenosine deaminase (ADA), superoxide dismutase (SOD), and catalase (CAT) activities and H. pylori.Ninety-nine patients were studied. Eight antral mucosal biopsies were taken for biochemical assessment of ADA, CAT, AND SOD activity and histological assessment. H. pylori density wAS evaluated according to the updated Sydney system. Patients were divided into three groups according to Sydney classification. ADA activity was found to be higher in patients having H. pylori in the present study. Also, ADA activity was higher in patients with a severe density of H. pylori. SOD level was found to be significantly higher with increased H. pylori density in our study (P < 0.05). In addition, SOD activity was higher in it H. Pylori-positive than H. pylori-negative patients. We did not find CAT activity in some antral tissue specimens. The significantly high levels of ADA activity in patients with H. pylori infection may reflect the regulator role of ADA in acid secretion. The higher ADA level with increased H. pylori density and H. pylori positivity indicate the probable malign lymphoid process of the stomach. But these findings must be confirmed with larger studies that include different gastric lesions.

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Section: Discussionmentioning

confidence: 99%

Association of Adenosine Deaminase, Superoxide Dismutase, and Catalase Activities with Helicobacter pylori

et al. 2005

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“…Previous studies have shown that the strains that produce the cytotoxin are also able to produce CagA, while the strains that do not produce the cytotoxin have the cytotoxin gene but lack the gene coding for CagA 2 . Antibody titres against CagA correlate with the severity of gastritis, suggesting a role of the CagA protein and the coexpressed cytotoxin in the pathogenesis of gastric lesions 8 , 9 . Recently, it has been reported that infection with cagA ‐positive H. pylori strains is associated with a higher degree of gastric inﬂammation, corresponding to an increased risk of peptic ulceration 10 and carcinogenesis 11 .…”

Section: Introductionmentioning

confidence: 99%

Augmented levels of gastric mucosal leucocyte activation by infection with cagA gene‐positive Helicobacter pylori

Suzuki

Mori

et al. 1998

J of Gastro and Hepatol

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The possession of the cytotoxin-associated gene (cagA) of Helicobacter pylori is thought to be highly associated with peptic ulcer disease. However, the pathogenic role of cagA is still unknown. We have emphasized the importance of the interrelationship between H. pylori-derived ammonia and oxygen radicals from infiltrated leucocytes. The aim of the present study was to explore the relationship between oxygen radical production and H. pylori strain diversity based on cagA possession. An endoscopic examination and gastric mucosal biopsy were performed in 30 H. pylori-infected patients with gastric ulcer. Myeloperoxidase (MPO) content and the luminol-dependent chemiluminescence value in the biopsied gastric specimens were measured as an index for leucocyte infiltration and oxygen radical production. From the precipitates of cultured bacterial isolates of biopsied specimens, bacterial DNA was purified and analysed by polymerase chain reaction to characterize the possession of cagA. While all patients had ureC-positive strains, 22 had cagA-positive and eight had cagA-negative strains. In patients with cagA-positive strains, MPO contents as well as chemiluminescence values in the gastric corpus were significantly higher than those in patients with cagA-negative strains. Gastric mucosal leucocyte recruitment and activation are suggested to be enhanced by cagA gene-positive H. pylori infection.

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“…Although confined primarily to the mucus layer overlying the gastric epithelial cells, naturally acquired infection elicits a vigorous local and systemic inflammatory and immune response, albeit a nonprotective one [55][56][57]. Electron microscopic evidence suggests that H. pylori has definite but limited invasive potential [58,59].…”

Section: Helicobacter Pylorimentioning

confidence: 99%