• Korean Journal of Microbiology
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• v.47 no.2
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• pp.124-129
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• 2011

The role of the ferric uptake regulator (Fur) of Helicobacter pylori in the oxidative stress was investigated in this study. A fur knockout mutant of H. pylori was constructed by replacing the fur gene with an aphA (kanamycin resistant marker) gene. Photodynamic therapy using methylene blue (MB) and 660 nm light was chosen to induce oxidative stress. The bactericidal effect of photodynamic therapy (PDT) was compared between wild type H. pylori and fur knockout mutant H. pylori. The degree of oxidative damage of DNA was confirmed using alkaline gel electrophoresis and an assay of 8-hydroxy-2-deoxyguanosine (8-OHdG). In control groups, the number of viable cells was maintained constantly during experiment. After PDT, the mutant H. pylori showed 10,000 times decreased viable cell number compared with wild type H. pylori. Depending on the exposure time of 660 nm light, the 3-fold increase in the concentration of 8-OHdG was observed in mutant H. pylori. The results of this study showed that H. pylori's Fur protein may play a role in oxidative stress induced by PDT.

• Journal of Oral Medicine and Pain
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• v.33 no.3
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• pp.241-246
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• 2008

Lichen planus is a common, chronic inflammatory disease of the skin and mucous membrane for which no precise causes have been confirmed. But it is often connected with infections. Helicobacter pylori(H. pylori) among various bacteria has been associated with the cause of gastritis, peptic ulcer and gastric cancer. Considering the similarities of histological features between gastric ulcer and oral ulcers, it is resonable to assume that H. pylori might also be involved in the development oral mucosal ulceration. So we employed this study to investigate the possible involvement of H. pylori in the aetiology of erosive oral lichen planus. We analyzed detection rate of H. pylori in saliva of patients with erosive oral lichen planus by nested PCR. As a result, it revealed a significant difference statistically by showing positivity in 16 to 21(76.2%) saliva samples of patients group and in 11 of 44(25%) saliva samples of control group(P>0.001). We were able to suppose that H. pylori in saliva can be related to cause of erosive oral lichen planus.

• Korean Journal of Veterinary Research
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• v.46 no.4
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• pp.327-335
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• 2006

A stable and reliable Helicobacter pylori (H. pylori) infection animal model would be necessary for evaluating vaccine efficacy and helpful for understanding the pathological mechanism of the organism. The aim of the present study is to investigate the effect of ethanol treatment prior to H. pylori inoculation on associated gastric mucosal injury and to establish ethanol-pretreating animal model to study H. pylori infection. Male Mongolian gerbils were used for the study. H. pylori was orally inoculated after 12 h fasting. 3 h prior to H. pylori inoculation, a group of gerbils was orally treated with absolute ethanol, 60% and 40% ethanol respectively. Another group of animals was treated either with H. pylori culture media alone or with different concentrations of ethanol plus culture media. Gerbils were killed 4 or 8 weeks after H. pylori inoculation. The colonization of H. pylori was confirmed by both histological examination and rapid urease test. Mucosal damage was evaluated grossly and histologically according to the criteria. The colonization of H. pylori and pathological changes in gastric mucosa of the animals were also observed. Although no significant change to the gastric mucose was observed in the animals treated either with H. pylori culture media alone or with different concentrations of ethanol plus culture media, persistent H. pylori infection was seen in the mucosa and mucosal leucocyte infiltration and severe epithelial damage was observed in the Helicobacter and ethanol + Helicobacter groups after 4 weeks. The gross and histological scores were higher in the ethanol + Helicobacter than in the Helicobacter alone group. As the results, ethanol-pretreatment with 60% concentration induced severe pathogenic changes by H. pylori infection in 5 weeks-old Mongolian gerbils. These results suggested that ethanol-pretreatment before H. pylori inoculation could increase the severity of gastric mucosal inflammation and enhance the colonization of H. pylori. The established ethanol-pretreating animal model would contribute to screen new drugs against H. pylori and be used as an useful tool for various animal experiments with H. pylori strains.

• Korean Journal of Clinical Laboratory Science
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• v.42 no.1
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• pp.38-45
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• 2010

The aim of this study was to assess the Clinical Usefulness of Helicobacter pylori Stool Antigen (HpSA) immunochromatographic assay for the diagnosis of H. pylori infection. In this study, we had compared HpSA-immunochromatographic assay with CLO test and UBT test. From a total of 140 patients (M:F=88:52) with upper endoscopy, biopsy specimens were obtained for CLO test. Stool specimens was collected from all patients and tested using a HpSA-immunochromatic assay. H. pylori infection status was defined as infected if the results of both CLO test and UBT test were positive. CLO test and UBT test findings showed that 92 patients were H. pylori positive and 48 patients were H. pylori negative. According to this definition, the sensitivity, specificity, and positive or negative predictive value (PPV, NPV) of HpSA-immunochromatographic assay were 97.8%, 100%, 100%, and 96%, respectively. Cross reactivity test of HpSA-immunochromatographic assay were performed with 10 enteric bacteria strains in fecal habitat, and there were no false positive reaction. We evaluated the usefulness of HpSA assay for eradication therapy with 10 of 92 H. pylori positive patients, positive results of them at pre-eradication therapy were converted to negative at post-eradication. The HpSA-immunochromatographic assay is a highly sensitive and specific non-invasive diagnostic method for detection of H. pylori infection, a useful diagnostic method for H. pylori in post eradication stage.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.1 no.1
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• pp.30-36
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• 1998

Purpose: It is well known that duodenal ulcer disease does not relapse if H. pylori is cleared from the gastric mucosa. Little is known about the recurrence of duodenal ulcer in children. The purpose of this study was to evaluate the effect of the eradication of H. pylori in duodenal ulcer in children upon the duodenal ulcer recurrence. Methods: 105 patients (M:F=78:27) diagnosed as duodenal ulcer by endoscopy in 1987~1995 were reviewed clinically, and were parted into two groups. The two treatment groups were ranitidine/antacid (RAN/ANT) and ranitidine/amoxicillin/denol (RAN/AMX/D). The latter was for H. pylori-positive children with duodenal ulcer who were diagnosed by serology and/or antral biopsies for histology, culture, and urease testing. The recurrence rates were compared between the two groups. Results: 1) 30 patients with primary duodenal ulcer underwent endoscopy for H. pylori and 27 (90.0%) of them were positive for H. pylori. 2) 27 of H. pylori-positive children received RAN/AMX/D. 23(85.2%) of them showed cure of duodenal ulcer and eradication of H. pylori. 3) The duodenal ulcer recurrence rate in RAN/ANT group was 65.3% and the rate in RAN/AMX/D was 4.3% by a year. Conclusions: There is a strong correlation between the duodenal ulceration and H. pylori infection in children, and the eradication of H. pylori in duodenal ulcer patients reduces the recurrence of the ulcer. Because of the low incidence of duodenal ulcers in children, a multicenter prospective study is required to determine the effect of treating H. pylori infetion on the long term natural history of duodenal ulcer disease.

• Journal of Gastric Cancer
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• v.2 no.2
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• pp.63-68
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• 2002

위의 parietal cell 혹은 대식세포와 유사한 세포 내부에서 H. pylori가 발견된다는 보고가 있기는 하나 일반적으로 H. pylori는 Shigella와 같은 침습성 세균은 아닌 것으로 알려져 있다. 그럼에도 불구하고 H. pylori에 감염된 위점막에는 많은 수의 호중구를 위시한 염증세포의 침윤이 관찰되는데 H. pylori가 위상피세포에 부착할 경우 위상피세포를 자극하여 interleukin-8을 위시한 cytokine을 발현케하고 이에 의하여 호중구 등의 염증세포가 몰려들게 된다. 한편 고유층에 몰려든 호중구에서는 다시 interleukin-8을 위시한 일련의 호중구 활성화 chemokine을 분비하여 염증반응을 증폭해 나갈 것이다. 호중구에서 발현되는 myeloperxidase나 활성산소 등도 위점막의 조직 손상에 기여할 것이다. 위상피세포를 덮고 있는 점액층은 위상피세포를 보호한다고 알려져 있으나 H. pylori 감염의 경우 점액층에 의하여 H. pylori의 운동성이 증가하고 이것이 위상피세포로부터의 cytokine 발현을 자극하여 염증반응을 증폭하는 데 관여할 가능성도 있다. H. pylori는 위상피세포에 대하여 apoptosis를 유도함과 동시에 고유층에 몰려든 호중구에 대하여는 apoptosis를 억제케하여 궁극적으로 염증반응을 증폭 및 지속시켜 나가는 쪽으로 작용한다. 한편 H. pylori는 위상피세로로부터 COX-2의 발현을 증가시키는데 이는 위상피세포의 APOPTOSIS를 억제하는 방향으로 작용한다. 이외에 H. pylori의 urease에 의하여 발생한 암모니아나 H. pylori 자신이 분비하는 세포독소가 세포 손상을 유발할 가능성도 있다. 상술한 여러 독성 인자들 중 어느 하나가 단독으로 작용하기보다는 여러 인자가 같이 동시에 또는 시차를 두고 작용할 가능성이 많다고 생각된다.

• Journal of Life Science
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• v.17 no.12
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• pp.1695-1700
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• 2007

The aim of this study was to estimate the ingestion effect of fermented soybean paste on the growth inhibition of Helicobacter pylori. Anti-H. pylori effect of the aqueous extract of soybean paste and cell-free supernatant of the isolates from soybean paste were determined using agar diffusion method. Soybean paste and the isolates inhibited the growth of H. pylori. Effect of soybean paste ingestion was estimated using urea breath test against infected volunteers showing no symptom of gastric disease. When 10 g of soybean paste was ingested 3 times a day for 6 weeks, average value of $P={\Delta}^{13}C(T_1-T_0)$ decreased from P=58 to P=28. This result indicated that fermented soybean paste was effective to inhibit the growth of H. pylori in gastric tissue.

• Journal of Periodontal and Implant Science
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• v.34 no.4
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• pp.723-731
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• 2004

Helicobacter pylori(H. pylori) has been associated with the cause of chronic gastritis, peptic ulcers and gastric cancer. Although it may be transmitted through the oral cavity, it is unknown whether the oral cavity acts as a reservoir of H. pylori. The purpose of this study was to investigate the mode of detection of H. pylori in oral cavity of adult periodontitis patients with plaque and periodontal pocket which atmosphere is grown well H. pylori. We analysed detection rate of H. pylori in saliva and subgingival plaques of 17 adult periodontitis patients without symptoms of gastroduodenal disease by nested PCR. Samples tested comprised saliva and subgingival plaques from central incisor, 1st premolar and 1st molar. H. pylori DNA was not identified in saliva from all patients. The detection rate in subgingival plaque from incisors, premolars and molars was 5.9%, 5.9% and 17.7%, respectively. In conclusion, the dental plaque and periodontal pocket (especially, of molars) in adult periodontitis can be favorable reservoir of H. pylori and may be the source of infection and transmission of H. pylori.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.22
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• pp.9905-9908
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• 2014

Background: Helicobacter pylori (H. pylori) is the most common chronic infectious agent in the stomach. Most importantly, it may lead to atrophy, metaplasia and cancer. The aim of this study was to investigate the incidence of H. pylori infection and to detect early mucosal changes that may lead to malignant degeneration in children. Materials and Methods: Children who underwent upper gastrointestinal endoscopy were included. Familial history of gastric cancer was noted. Endoscopic examinations were performed by a single pediatric gastroenterologist. A minimum of three biopsy samples were collected during endoscopy. The patients were accepted as H. pylori infected if results of biopsies and rapid urease test were both positive. Biopsies were evaluated for the presence and degree of chronic inflammation, the activity and severity of gastritis, glandular atrophy and intestinal metaplasia. Results: A total of 750 children (388 boys, 362 girls) were evaluated in our study, with a mean age of 10.1 years. A total of 390 patients (52%) were found to be infected with H. pylori. Among the H. pylori infected patients, 289 (74%) were diagnosed to have chronic superficial gastritis, 24 (6.2%) had gastric atrophy. Most strikingly, intestinal metaplasia was observed in 11 children, all were in the H. pylori positive group. There was no difference in the mean of age, gender and socioeconomic class between H. pylori infected and non-infected groups. The frequency of gastric cancer in family members (4 in number) was higher in patients with H. pylori infection. No gastric cancer case was reported from the parents of non-infected children. The worst biopsy parameters (atropy and metaplasia) were improved after H. pylori eradication on control endoscopy. Conclusions: The current study shows a higher prevalence of familial history of gastric cancer in H. pylori infected children. Intestinal metaplasia was also higher in the infected children. Eradication of H. pylori infection for this risk group may prevent subsequent development of gastric cancer.

• Korean Journal of Microbiology
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• v.41 no.2
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• pp.152-156
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• 2005

In the present study, lactic acid bacterium that has antibacterial activity against Helicobacter pylori was isolated from feces of newborn baby. The selection was based on the ability to inhibit the growth of H. pylori and to withstand harsh environmental conditions such as acidic pH and high bile concentration. By biochemical test and 16S rDNA sequencing, selected strain was turned out to be an Pediococcus acidilactici, therefore designated to P. acidilactici GMB7330. In order to investigate the inhibitory effects of P. acidilactici GMB7330 on the growth of H. pylori, we have tested in vitro studies such as cell viability and urease test. These results showed that antibacterial activity of P. acidilactici GMB7330 significantly decreased the viable cell count and urease activity of H. pylori. Antibacterial activity of P. acidilactici GMB7330 against H. pylori remained after pH adjustment to neutral, and the concentration of lactate produced from P. acidilactici GMB7330 was not enough to inhibit H. pylori. On the basis of the analysis by transmission electron microscope, it demonstrated that addition of P. acidilactici GMB7330 destroyed the cell structure of H. pylori. These results strongly suggested that P. acidilactici GMB7330 produce antibacterial substances to be able to inhibit the growth of H. pylori other than lactic acid.