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DOI 10.1111/j.1440-1746.1998.01558.x

Медицинская библиотека · Journal of gastroenterology and hepatology · 1998

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

Suzuki H, Suzuki M, Mori M, Kitahora T, Yokoyama H, Miura S, Hibi T, Ishii H

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

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.

Для цитирования: Suzuki H, Suzuki M, Mori M, Kitahora T, Yokoyama H, Miura S, Hibi T, Ishii H. Augmented levels of gastric mucosal leucocyte activation by infection with cagA gene-positive Helicobacter pylori.. Journal of gastroenterology and hepatology. 1998. DOI: 10.1111/j.1440-1746.1998.01558.x.

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