• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.13 no.1
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• pp.7-22
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• 2010

Purpose: Nodular gastritis is a characteristic finding of Helicobacter pylori infection in children. The aim of this study was to evaluate the difference in gene expression in the gastric mucosa of H. pylori-infected and non-infected children, and to analyze the difference in gene expression using cDNA microarray analysis of nodular gastritis caused by H. pylori infection. Methods: Twelve children (6 boys and 6 girls; mean age 9.8 years) who underwent upper gastrointestinal endoscopy and biopsy at Seoul National University Bundang Hospital were included in the study. The subjects were divided into three groups according to the presence of H. pylori infection and nodular gastritis on endoscopic examination. Gastric mucosa tissue was kept at $-70^{\circ}C$ and RNA was extracted to perform cDNA microarray analysis in each patient. Results: cDNA microarray analysis in children revealed a clear distinction between H. pylori-infected and non-infected gastric mucosa. Specifically, 182 over-expressed genes and 29 under-expressed genes were identified in H. pylori-infected gastric mucosa compared to non-infected mucosa. H. pylori-infected nodular gastritis revealed different gene expression patterns from H. pylori-infected normal gastric mucosa; five genes were over-expressed and five genes were under-expressed. Conclusion: In the presence of H. pylori infection, gastric mucosa shows distinct differences in gene expression, and nodular gastritis with H. pylori infection in children may be associated with over- or under-expression of some genes. Further studies are required to clarify the host response and the pathogenesis of nodular gastritis in children.

• Microbiology and Biotechnology Letters
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• v.25 no.3
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• pp.240-247
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• 1997

Bacillary is the most common form of H. pylori observed during human infection. However, it is known that the morphology change of H. pylori from bacillary to coccoid can be occurred with a response to the environmental stresses such as the nutrient depletion, accumulation of toxic metabolites, pH alteration, and exposure to antimicrobial agents. The coccoid form of H. pylori, which is viable but non-culturable in vitro, seems to be the major cause of antibiotic resistancy and high reinfectability of H. pylori. In this regard, we studied the environmental factors that can induce the morphological change in vitro of H. pylori, and the change of fatty acid composition of plasma membrane. The morphological change from bacillary to coccoid could be observed with the depletion of nutrients, pH variation and reactive oxygen species added in the culture media. This morphologic conversion was paralleled by a dramatic decrease in unsaturated fatty acids and an increase in saturated fattv acids of plasma membrane. The change in composition of membrane fatty acid seems to be a kind of protection mechanism of H. pylori against these environmental stresses.

• 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.

• Nutrition Research and Practice
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• v.11 no.1
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• pp.11-16
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• 2017

BACKGROUND/OBJECTIVES: Helicobacter pylori (H. pylori) colonization of the stomach mucosa and duodenum is the major cause of acute and chronic gastroduodenal pathology in humans. Efforts to find effective anti-bacterial strategies against H. pylori for the non-antibiotic control of H. pylori infection are urgently required. In this study, we used whey to prepare glycomacropeptide (GMP), from which sialic acid (G-SA) was enzymatically isolated. We investigated the anti-bacterial effects of G-SA against H. pylori in vitro and in an H. pylori-infected murine model. MATERIALS/METHODS: The anti-bacterial activity of G-SA was measured in vitro using the macrodilution method, and interleukin-8 (IL-8) production was measured in H. pylori and AGS cell co-cultures by ELISA. For in vivo study, G-SA 5 g/kg body weight (bw)/day and H. pylori were administered to mice three times over one week. After one week, G-SA 5 g/kg bw/day alone was administered every day for one week. Tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), IL-$1{\beta}$, IL-6, and IL-10 levels were measured by ELISA to determine the anti-inflammatory effects of G-SA. In addition, real-time PCR was performed to measure the genetic expression of cytotoxin-associated gene A (cagA). RESULTS: G-SA inhibited the growth of H. pylori and suppressed IL-8 production in H. pylori and in AGS cell co-cultures in vitro. In the in vivo assay, administration of G-SA reduced levels of IL-$1{\beta}$ and IL-6 pro-inflammatory cytokines whereas IL-10 level increased. Also, G-SA suppressed the expression of cagA in the stomach of H. pylori-infected mice. CONCLUSION: G-SA possesses anti-H. pylori activity as well as an anti-H. pylori-induced gastric inflammatory effect in an experimental H. pylori-infected murine model. G-SA has potential as an alternative to antibiotics for the prevention of H. pylori infection and H. pylori-induced gastric disease prevention.

• Nutritional Sciences
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• v.9 no.3
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• pp.152-158
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• 2006

Helicobacter pylori (H. pylori) infection rapidly stimulated either COX-2 or 5-LOX and released arachidonic acid metabolites that have been considered as pivotal mediators in H. pylori-induced inflammatory responses. To determine whether red ginseng extract (RGE) can suppress the biosynthesis of 5(S)-hydroxyeicosatetraenoic acids (HETE), a precursor metabolite of leukotrienes B4 (LTB4) in H. pylori-provoked inflammatory responses in gastric epithelial cells, the biosynthesis of monohydroxy fatty acids was measured using radioactive arachidonic acid and validated by RP-HPLC using non-radioactive AA as substrate in AGS cells cocultured with H. pylori (ATCC 43504) with or without pretreatment of RGE. Among three known major HETEs, H. pylori infection specifically induced the biosynthesis of $^{14}C-5(S)-HETE$ rather than the complex of $^{14}C-15S-/^{14}C-12(S)-HETE$ from $^{14}C-AA$, concomitantly obtained by HPLC(p<0.01). RGE, 1 to $100{\mu}g/ml$, selectively suppressed H. pylori-stimulated $^{14}C-5(S)-HETE$ production implying the attenuation of 5-lipoxygenase activity, of which was similar to known LOX inhibitor NDGA $(10{\mu}M)$ (p<0.01). However, the amount of 5(S)-HETE was significantly reduced by higher dose of RGE $(100{\mu}g/ml)$ (p<0.05). These results indicated that LOX pathway might be one of principle pathogenic mechanisms of H. pylori and red ginseng could be a nutraceutical against H. pylori infection through inhibiting action of LOX activity.

• 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.

• Clinical Endoscopy
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• v.56 no.1
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• pp.75-82
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• 2023

Background/Aims: The etiology of superficial non-ampullary duodenal epithelial tumors (SNADETs) remains unclear. Recent studies have reported conflicting associations between duodenal tumor development and Helicobacter pylori infection or endoscopic gastric mucosal atrophy. As such, the present study aimed to clarify the relationship between SNADETs and H. pylori infection and/or endoscopic gastric mucosal atrophy. Methods: This retrospective case-control study reviewed data from 177 consecutive patients with SNADETs who underwent endoscopic or surgical resection at seven institutions in Japan over a three-year period. The prevalence of endoscopic gastric mucosal atrophy and the status of H. pylori infection were compared in 531 sex- and age-matched controls selected from screening endoscopies at two of the seven participating institutions. Results: For H. pylori infection, 85 of 177 (48.0%) patients exhibited SNADETs and 112 of 531 (21.1%) control patients were non-infected (p<0.001). Non-atrophic mucosa (C0 to C1) was observed in 96 of 177 (54.2%) patients with SNADETs and 112 of 531 (21.1%) control patients (p<0.001). Conditional logistic regression analysis revealed that non-atrophic gastric mucosa was an independent risk factor for SNADETs (odds ratio, 5.10; 95% confidence interval, 2.44-8.40; p<0.001). Conclusions: Non-atrophic gastric mucosa, regardless of H. pylori infection status, was a factor independently associated with SNADETs.

• 한국생물공학회:학술대회논문집
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• 2000.11a
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• pp.264-265
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• 2000

Helicobacter pylori(H. pylori) is the causative agent of chronic gastritis and the single most important factor in peptic ulcer disease, however, the pathogenetic mechanisms underlying H, pylori infection are not well understood. Futhermore, there is a strong association between H. pylori infection and gastric cancer. Various diagnostic methods for detecting H. pylori infection are available. These can be divided into invasive methods, requiring endoscopy, and non-invasive tests, mainly 13C-urea breath tests and serologic detection of antibodies. Rapid urease test is the most recommendable endoscopic test for the diagnosis of H. pylori infection, presently. CLO test kit is the represent of rapid urease test kits. The principles of CLO test kit is that hydrolysis of urea by urease Is detected by a dye indicators showing a color change. Our device is used same principle but we improved the reaction time is more faster and positive color change is more distinctive from the color of the negative specimen. So, this kit is more reliable because it response faster and accuracy.

• Korean Journal of Clinical Laboratory Science
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• v.39 no.3
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• pp.271-276
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• 2007

Helicobacter pylori (H. pylori) infection is common in korea and high incidence at gastric ulcer and duodenal ulcer. $^{14}C-urea$ breath test ($^{14}C-UBT$) is regarded as a highly reliable and non-invasive method for the diagnosis of H. pylori infection. The purpose of this study was to evaluate the diagnositc performance of a new and rapid $^{14}C-UBT$, which was equipped with Geiger-Muller counter and compared the results with those obtained by gastroduodenoscopic biopsies (GBx). One hundred sixty-eight patients (M : F = 118 : 50) underwent $^{14}C-UBT$, rapid urease test (CLO test), and GBx. The results of $^{14}C-UBT$ were classified as positive (>50 cpm), borderline (25$^{14}C-UBT$ or CLO test results with GBx as a glod standard. In the assessment of the presence of H. pylori infection, the $^{14}C-UBT$ global performance yielded positive predictive value, negative predictive value and accuracy of 93.3% and 83.3%, respectively. However, the CLO test had performance yielded positive predictive value, negative predictive value and accuracy of 76.9%, 50.0%, respectively. In this study $^{14}C-UBT$ is a highly accurate, simple and non-invasive method or the diagnosis of follow up H. pylori infection.

• Journal of Gastric Cancer
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• v.24 no.1
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• pp.99-107
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• 2024

Gastric cancer has been consistently decreasing worldwide, whereas cardia gastric cancer is on the rise. This indicates that the exposure rates to epidemiological causes are changing. In this study, we aim to review the risk factors for gastric cancer with respect to cardia and non-cardia types. One of the most significant risk factors for gastric cancer is Helicobacter pylori infection. H. pylori infection is known as a risk factor for non-cardia gastric cancer, and there have been results indicating that H. pylori infection is not associated with cardia gastric cancer. However, in the East Asian region, there is epidemiological evidence suggesting that H. pylori infection might be a risk factor for cardia gastric cancer. Smoking and alcohol consumption are known risk factors for gastric cancer, regardless of anatomical location. Obesity is considered a factor in the development of cardia gastric cancer. However, further research is needed to understand the specific relationship with non-cardia gastric cancer. The consumption of high-salt and processed meat is more distinctly associated with noncardia gastric cancer than in cardia gastric cancer. In addition to these factors, exposure to chemicals and radiation are considered risk factors for gastric cancer. Primary prevention of gastric cancer involves eliminating or avoiding risk factors such as H. pylori eradication and adopting a healthy lifestyle, including quitting smoking, reducing alcohol consumption, maintaining a healthy weight, and having a low-salt diet.