Ryuzo Deguchi

Effect of pretreatment with Lactobacillus gasseri OLL2716 on first-line Helicobacter pylori eradication therapy.

Background and Aim:  Helicobacter pylori eradication clearly decreases peptic ulcer recurrence rates. H. pylori eradication is achieved in 70–90% of cases, but treatment failures due to poor patient compliance and resistant organisms do occur. Lactobacillus gasseri can suppress both clarithromycin‐susceptible and ‐resistant strains of H. pylori in vitro. The aim of this study was to determine the effect of pretreatment with L. gasseri‐ containing yogurt on H. pylori eradication. We conducted a randomized, controlled clinical trial in patients with H. pylori infection.

The effect of Helicobacter pylori on cell proliferation and apoptosis in gastric epithelial cell lines

Background: Helicobacter pylori has been implicated in the pathogenesis of gastric cancer and malignant lymphoma. It is not known whether the bacterium stimulates cell proliferation directly or if apoptosis induced by H. pylori leads to a hyperproliferative response.

Association between CagA+Helicobacter pylori infection andp53,bax andtransforming growth factor-?-RII gene mutations in gastric cancer patients

We assessed the possible association between CagA+ Helicobacter pylori infection and gastric carcinogenesis in gastric cancer patients. Gastric biopsy specimens were obtained from 64 patients with gastric cancer and were histologically classified into intestinal and diffuse types. H. pylori infection was determined by cultivation, flaA‐PCR and serum antibody against CagA. p53, BAX and transforming growth factor‐β‐RII (TGFβ‐RII) gene mutations were analyzed by PCR‐SSCP and direct sequencing. Intestinal and diffuse types of cancer were detected in 45 and 19 patients, respectively. H. pylori infection was found in 55 (85.9%) of 64 patients. There was no significant difference in H. pylori positivity between intestinal and diffuse types. However, the CagA antibody was positive in 15 (78.9%) of 19 patients with the diffuse type and in 22 (48.9%) of 45 patients with the intestinal type (p = 0.030). Among the 55 H. pylori‐positive cases, 11 (29.7%) of the 37 patients in the CagA+ group were found to have p53 alterations, compared with 2 (11.1%) in the 18 CagA‐ group (p = 0.182). Moreover, among the 64 gastric cancer patients, p53 alterations were more frequently found in the CagA+ group (29.7%) than in the H. pylori‐positive CagA‐ and H. pylori‐negative groups (7.4%; p = 0.033). BAX gene mutations were found in 19 (29.7%) of 64 patients and there was no relationship among CagA seropositivity, cancer stages and histopathological phenotypes. In contrast, the TGFβ‐RII gene mutation was only detected in one CagA‐ patient. The results suggest that CagA+ H. pylori infection may have an important role in the development of gastric cancer patients with p53 mutations

Relationship between IL-1β gene polymorphism and gastric mucosal IL-1β levels in patients with Helicobacter pylori infection

BackgroundInterkeukin-1 (IL-1) gene cluster polymorphisms that are thought to enhance the production of IL-1β are associated with an increased risk of gastric cancer. To determine the role of host genetic factors in Helicobacter pylori infection, we examined the relationship between gastric mucosal IL-1β levels and IL-1B polymorphisms in patients with H. pylori infection.MethodsBiopsy tissues obtained from 99 patients were homogenized and gastric mucosal IL-1β levels were measured by enzyme-linked immunosorbent assay (ELISA). Single-base polymorphisms at positions −511 and −31 in IL-1B were analyzed.ResultsThe IL-1β level in the antrum was significantly higher in genotype IL-1B-511C/C than in H. pylori-negative patients (P < 0.05). The IL-1B polymorphism did not influence the degree of gastric neutrophil and mononuclear cell infiltration, or gastric atrophy. IL-1β levels in the corpus, but not those in the antrum, correlated to the severity of gastric atrophy.ConclusionsThese findings indicate that IL-1B polymorphisms enhance IL-1β production in the antrum; however, other factors might regulate the production of IL-1β in the corpus of the stomach, regardless of IL-1B polymorphisms, and high IL-1β production may be associated with the grade of gastric atrophy in the corpus mucosa in patients with H. pylori infection.

Tetracycline, metronidazole and amoxicillin-metronidazole combinations in proton pump inhibitor-based triple therapies are equally effective as alternative therapies against Helicobacter pylori infection.

Background:  A proton pump inhibitor (PPI)‐based triple therapy with clarithromycin (CAM) and amoxicillin (AMPC) is now a standard regimen for Helicobacter pylori (HP) eradication in Japan. However, the CAM‐resistant rate has increased recently and alternative therapies are sorely needed. Therefore the aim of the present study was to evaluate the effectiveness and safety of the PPI–tetracycline (TC)–metronidazole (MNZ) regimen (the PTM regimen) as an alternative therapy in comparison with the PPI–AMPC–MNZ (PAM) regimen.

Clinical symptoms of FSSG in gastroesophageal reflux disease are critical for PPI treatment: Japanese multi-centers with 185 patients

Aim:  The main aim of this study was to determine whether questionnaire evaluations of clinical symptoms in gastroesophageal reflux disease were useful to assess proton pump inhibitor therapy.

Analysis of the cag pathogenicity island and IS605 of Helicobacter pylori strains isolated from patients with gastric cancer in Japan

Background : CagA protein is encoded by the cagA gene, which is part of the cag pathogenicity island (PAI) in Helicobacter pylori. Insertion sequence (IS) elements are a diverse set of specialized DNA segments that can move to new sites in bacterial genomes.

Analysis of Helicobacter pylori and nonsteroidal anti‐inflammatory drug‐induced gastric epithelial injury

Helicobacter pylori and nonsteroidal anti‐inflammatory drugs (NSAIDs) are important factors in gastric mucosal injury. However, the relationship between H. pylori and NSAID‐related gastroduodenal mucosal injury has not been clarified.

Interaction between Helicobacter pylori and immune response to CagA: CagA antibody may down-regulate bacterial colonization and tyrosine phosphorylation: INTERACTION BETWEEN H. PYLORI AND IMMUNE RESPONSE TO CAGA

CagA+Helicobacter pylori strains are associated with the development of gastroduodenal diseases. H. pylori possess a type IV secretion system that is responsible for the translocation of CagA into host cells.