• Preventive Nutrition and Food Science
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• v.9 no.2
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• pp.161-166
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• 2004

The effects of kimchis intake on Helicobacter pylori infection in the stomach, the counts of lactic acid bacteria in the large intestine, and bacterial enzymes ($\beta$-glucosidase, $\beta$-glucuronidase) and pH in feces were examined. A total of 20 participants (age range 34 ∼ 57) were assessed for H. pylori infection status by Be urea breath test. Fourteen participants were eliminated because they were H. pylori-negative. This study consisted of 4 consecutive phase, each of which lasted 4 weeks. Three hundred grams of kimchi were administered to H. pylori-infected subjects during the kimchi phase, followed by 4 weeks of control phase. During the control phase, subjects consumed 60 g of kimchi, the minimum amount in their customary diets. All participants were found to be H. pylori-positive during all experimental periods. During the kimchi phase, delta over baseline (DOB) level was lower than during the control phase, although significant difference between the kimchi and control phases were not found (p=0.9439). However, the counts of Lactobacillus sp. and Leuconostoc sp. significantly (p < 0.0005) increased during the kimchi phase. $\beta$-Glucosidase and $\beta$-glucuronidase activities and pH were significantly decreased by kimchi intake compared to control (p=0.000l). These results suggested that kimchi consumption did not show any therapeutic effect on H. pylori in the stomach. However, kimchi seemed to be a good food for colon health, since it increased the beneficial bacteria such as lactobacillus and decreased toxic enzyme ($\beta$-glucosidase and $\beta$-glucuronidase) activity and pH.

• Journal of Gastric Cancer
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• v.8 no.3
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• pp.113-119
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• 2008

Purpose: This study investigated whether a single nucleotide polymorphism (SNP) located at position -2 in the Kozak sequence of the TFF1 gene is associated with H. pylori infection and the development of gastric cancer in Koreans. Materials and Methods: We enrolled 167 patients with gastric cancer from January 2000 to December 2003 and also 299 healthy controls during the same period. The genotype of the TFF1 SNP was analyzed by polymerase chain reaction-restriction fragment length polymorphism and single strand conformation polymorphism. We also examined the H. pylori infection by Giemsa staining. Results: No significant difference in the allele or the TFF1 SNP genotype frequency was observed between the patients with gastric cancer and the control subjects (P=0.595 and P=0.715, respectively). When stratified by the histological subtype of gastric cancer and the age of the patients, the risk was not statistically significant between the two study groups (P=0.088 and P=0.551, respectively). H. pylori infection was detected in 39 cases and it was not associated with the TFF1 genotype. Conclusion: These findings suggest that this TFF1 gene polymorphism is not associated with H. pylori infection and gastric cancer in Koreans and so it doesn't contribute to the susceptibility to gastric cancer in Koreans.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.5
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• pp.2351-2360
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• 2016

Management of Helicobacter pylori infection is an important aspect of many upper gastrointestinal tract diseases, such as chronic gastritis, peptic ulcer disease, gastric cancer and mucosa-associated lymphoid tissue (MALT) lymphoma. The Thailand Consensus on H. pylori treatment 2015 consisted of 22 national experts who took active roles, discussed all important clinical information and investigated clinical aspects in four workshops, focuising on: (1) Diagnosis (2) Treatment (3) Follow-up after eradication and (4) H. pylori infection and special conditions. Experts were invited to participate on the basis of their expertise and contribution to H. pylori works and/or consensus methodology. The results of each workshop were taken to a final consensus vote by all experts. Recommendations were developed from the best evidence and availability to guide clinicians in management of this specific infection associated with variety of clinical outcomes.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.11 no.sup1
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• pp.83-92
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• 2008

Helicobacter pylori is the causative agent of chronic gastritis and has a role in the pathogenesis of peptic ulcer diseases, and gastric cancer. There have been reports suggesting a close link between these gastroduodenal disorders and a state of vitamin C deficiency. In this paper, the past, present and future perspectives on H. pylori infection and vitamin C will be discussed under the following view points. Since the ecological niche of H. pylori is the mucus layer and intercellular junctions of the gastric epithelium, the various kinds of host inflammatory cells motivated by the local and systemic immune responses cannot eliminate the microorganisms. When the invading foreign body is not removed, despite full activation of defense mechanisms, adverse consequences of the immune responses develop on the host gastric mucosa. The reasons for the body vitamin C depletion could be explained as follows; 1) the increased vitamin C consumption by increased oxygen free radical production through the prolonged hypersensitivity reactions in the gastric mucosa, 2) the increased vitamin C oxidation by the nitrite which is formed from nitrate reduction by the intragastric bacteria proliferated in the hypochlorhydric gastric cavity, 3) the strong ${\gamma}$-glutamyltranspeptidase activity of H. pylori which depletes the glutathiones in gastric mucosa. Depletion of glutathiones in the stomach favors irreversible oxidative destruction of ascorbic acid. Both persistent inflammatory burdens in the stomach by H. pylori and resultant vitamin C depletions synergistically and uninhibitedly might aggravate the hypothetical sequence of gastric carcinogenesis: atrophic gastritis${\rightarrow}$intestinal metaplasia${\rightarrow}$dysplasia${\rightarrow}$gastric adenocarcinoma. High intake of vitamin C could reverse the hypothetical sequence of the gastric carcinogenesis via direct and indirect effects on H. pylori and host-parasite relationships.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.12 no.2
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• pp.140-149
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• 2009

Purpose: Helicobacter pylori infection is probably acquired in childhood and persists as an asymptomatic infection for decades in most individuals. It is unclear why only a minority of those infected develop a clinical manifestation, even in childhood, such as peptic ulcer disease. H. pylori infection activates local immune responses and causes lymphocyte infiltration in the gastric mucosa. We have previously reported that both T and B cells in the lamina propria play important roles in the local immune response of H. pylori-infected children. The aim of this study was to investigate the association between H. pylori genotypes and gastric mucosal lymphocytes. Methods: Twenty-five H. pylori-infected children (10 with peptic ulcer disease and 15 with gastritis) were enrolled in this study. We investigated the genotypes (cagA, cagE, vacA, and babA2) and evaluated the association with clinical manifestations, histopathology, and gastric mucosal lymphocytes. Results: The prevalence of cagA, cagE, vacA s1m1, and babA2 was 80%, 60%, 84%, and 88%, respectively. The most prevalent (68%) combination of cagA, vacA, and babA2 genotypes was cagA+/vacA s1m1+/babA2+. H. pylori genotypes were not associated with clinical manifestations, histopathology, or gastric mucosal lymphocytes. Conclusion: There was no association between the cagA, cagE, vacA, or babA2 status and gastric mucosal lymphocytes. The role of the host immune response in relation to H. pylori genotypes and disease potential in children needs further studies.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.7 no.2
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• pp.153-162
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• 2004

Purpose: The Helicobacter pylori stool antigen (HpSA) enzyme immunoassay is a non-invasive test for the diagnosis and monitoring of H. pylori infection. But, there are few validation studies on the HpSA test after eradication in children. The aim of this study was to assess the diagnostic accuracy of HpSA enzyme immunoassay for the detection of H. pylori to confirm eradication in children. Methods: From January 2001 to October 2003, 164 tests were performed in 146 children aged 1 to 17.5 years (mean $9.3{\pm}4.3$ years). H. pylori infection was confirmed by endoscopy-based tests (rapid urease test, histology, and culture). All H. pylori infected children were treated with quadruple regimens (Omeprazole, amoxicillin, metronidazole and bismuth subcitrate for 7 days). Stool specimens were collected from all patients for the HpSA enzyme immunoassay (Primier platinum HpSA). The results of HpSA tests were interpreted as positive for $OD{\geq}0.160$, unresolved for $$0.140{\leq_-}OD$$<0.160, and negative for OD<0.140 at 450 nm on spectrophotometer. Results: 1) One hundred thirty-one HpSA tests were performed before treatment. The result of HpSA enzyme immunoassay showed three false positive cases and one false negative case. The sensitivity, specificity, positive predictive value, and negative predictive value of HpSA enzyme immunoassay before treatment were 96.4%, 97.1%, 90%, and 99%, respectively. 2) Thirty-three HpSA enzyme immunoassay were performed at least 4 weeks after eradication therapy. The results of HpSA enzyme immunoassay showed two false positive cases and one false negative case. The sensitivity, specificity, positive predictive value, and negative predictive value after treatment were 88.9%, 91.7%, 80%, and 95.7%, respectively. Conclusion: Diagnostic accuracy of the HpSA enzyme immunoassay after eradication therapy was as high as that of the HpSA test before eradication therapy. The HpSA enzyme immunoassay was found to be a useful non-invasive method to confirm H. pylori eradication in children.

• Journal of Applied Biological Chemistry
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• v.58 no.1
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• pp.89-95
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• 2015

Helicobacter pylori infection causes gastrointestinal diseases such as chronic gastritis, peptic ulcers, and may lead to gastric cancer. Several studies have reported that lactobacilli present on broccoli show inhibitory activity against H. pylori. Here, we evaluated aqueous broccoli, fermented by Lactobacillus plantarum MG208, for its fermentation characteristics and anti-H. pylori activities including antibacterial activity, growth inhibition, anti-adhesion, and urease inhibition. The results indicated that the fermentation characteristics changed significantly depending on the amount of aqueous broccoli used for fermentation (p <0.05). There was no significant difference between the samples before fermentation (p >0.05). However, a significant concentration-dependent difference was noted in antibacterial activity and urease inhibition (p <0.05) following the addition of aqueous broccoli. Growth inhibition in the 10 mg/mL sample was significantly higher as compared to the negative control and similar to that with amoxicillin (positive control) (p <0.05). Anti-adhesion activity of aqueous broccoli was also significantly different (p <0.05) from the negative control. Therefore, aqueous broccoli fermented by L. plantarum MG208 could prove useful as a functional diet for protection of the gastric environment against H. pylori infection.

• The Korean Journal of Gastroenterology
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• v.72 no.5
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• pp.237-244
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• 2018

While the prevalence of Helicobacter pylori (H. pylori) infection is decreasing in Korea, the incidence of gastric cancer remains high, emphasizing the importance of H. pylori eradication. A new treatment strategy is needed as the eradication rate with standard triple therapy, which is currently the standard first-line regimen for H. pylori infection, has decreased below the optimum level. The major cause of eradication failure is increased antibiotic resistance. Sequential, concurrent, and hybrid therapies that include clarithromycin produce higher eradication rates than conventional standard triple therapy. However, the effectiveness of these treatments is limited in regions where the resistance rate to various antibiotics is high. Bismuth quadruple therapy is another alternative therapy, but again the eradication rate is not sufficiently high. Tailored therapy based on individual characteristics, including antibiotic susceptibility, may be ideal, but there are several limitations for clinical application and further research is needed. New potassium-competitive acid blocker-based therapies could emerge as effective alternatives in the near future. A consensus is needed to establish a strategy for applying new eradication therapies in Korea.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.8 no.1
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• pp.12-20
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• 2005

Purpose: Helicobacter pylori infection is known to be associated with acute or chronic abdominal pain and upper gastrointestinal bleeding in children. This study was performed to analyze the gastroduodenoscopic findings and the efficacy of triple therapy with omeprazole, amoxicillin and clarithromycin between one and two weeks of duration in children with H. pylori infection. Methods: We have assessed retrospectively 60 patients presented with acute or chronic abdominal pain or upper gastrointestinal bleeding. H. pylori infection was confirmed by endoscopic biopsy and rapid urease test. Out of 60 patients, 30 patients were treated with a combination of omeprazole, amoxicillin, and clarithromycin for one week, and the other 30 patients were treated for two weeks with the same medication. Efficacy of treatment was assessed 4 weeks after the termination of treatment by using the $^{13}C$ urea breath test. Results: The 60 patients with the complaint of diffuse abdominal pain, epigastric pain, vomiting or hematemesis were included in this study. One-week treatment group (group I) consisted of 30 patients (14 male, 16 female) with mean age of $11.6{\pm}2.67years$. Two-week treatment group (group II) consisted of 30 patients (11 male, 19 female) with mean age of $10.7{\pm}4.17years$. In group I, H pylori were eradicated in 26 out of 30 patients (86.7%). In group II, H. pylori were eradicated in 26 out of 30 children (86.7%). Both groups did $^{13}C$ urea breath test after 4 weeks after termination of the triple therapy. The eradication rates were same in both groups as 86.7%, 26 out of 30 patients in each group. The results of endoscopy were nodular gastritis 26 (43.3%), erosive gastritis 10 (16.7%), hemorrhagic gastritis 7 (11.7%), gastric ulcer 2 (3.3%) and normal finding 15 (25.0%). Conclusion: In this study, the nodular gastritis was most common endoscopic findings with H. pylori positive patients. The eradication rate of H. pylori with omeprazole, amoxicillin and clarithromycin was 86.7% and it would be highly effective as primary treatment with no significant differences in the eradication rate between one-week and two-week treatment groups. However, we should need more long-term follow-up data.

• Journal of Periodontal and Implant Science
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• v.49 no.3
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• pp.138-147
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• 2019

Purpose: Several studies have shown that the oral cavity is a secondary location for Helicobacter pylori colonization and that H. pylori is associated with the severity of periodontitis. This study investigated whether H. pylori had an effect on the periodontium. We established an invasion model of a standard strain of H. pylori in human periodontal ligament fibroblasts (hPDLFs), and evaluated the effects of H. pylori on cell proliferation and cell cycle progression. Methods: Different concentrations of H. pylori were used to infect hPDLFs, with 6 hours of co-culture. The multiplicity of infection in the low- and high-concentration groups was 10:1 and 100:1, respectively. The Cell Counting Kit-8 method and Ki-67 immunofluorescence were used to detect cell proliferation. Flow cytometry, quantitative real-time polymerase chain reaction, and western blots were used to detect cell cycle progression. In the high-concentration group, the invasion of H. pylori was observed by transmission electron microscopy. Results: It was found that H. pylori invaded the fibroblasts, with cytoplasmic localization. Analyses of cell proliferation and flow cytometry showed that H. pylori inhibited the proliferation of periodontal fibroblasts by causing G2 phase arrest. The inhibition of proliferation and G2 phase arrest were more obvious in the high-concentration group. In the low-concentration group, the G2 phase regulatory factors cyclin dependent kinase 1 (CDK1) and cell division cycle 25C (Cdc25C) were upregulated, while cyclin B1 was inhibited. However, in the high-concentration group, cyclin B1 was upregulated and CDK1 was inhibited. Furthermore, the deactivated states of tyrosine phosphorylation of CDK1 (CDK1-Y15) and serine phosphorylation of Cdc25C (Cdc25C-S216) were upregulated after H. pylori infection. Conclusions: In our model, H. pylori inhibited the proliferation of hPDLFs and exerted an invasive effect, causing G2 phase arrest via the Cdc25C/CDK1/cyclin B1 signaling cascade. Its inhibitory effect on proliferation was stronger in the high-concentration group.