• Asian Pacific Journal of Cancer Prevention
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• 제16권18호
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• pp.8281-8285
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• 2016

Background: Helicobacter pylori is a cause of chronic gastritis, peptic ulcer disease, and gastric malignancy, infection being a serious health problem in Thailand. Recently, clarithromycin resistant H. pylori strains represent the main cause of treatment failure. Therefore this study aimed to determine the prevalence and pattern of H. pylori resistance to clarithromycin in Suranaree University of Technology Hospital, Suranree University of Technology, Nakhon Ratchasima, Northeastern Thailand, Nakhon Ratchasima province, northeast of Thailand. Materials and Methods: This hospital-based cross-sectional study was carried out between June 2014 and February 2015 with 300 infected patients interviewed and from whom gastric mucosa specimens were collected and proven positive by histology. The gastric mucosa specimens were tested for H. pylori and clarithromycin resistance by 23S ribosomal RNA point mutations analysis using real-time polymerase chain reactions. Correlation of eradication rates with patterns of mutation were analyzed by chi-square test. Results: Of 300 infected patients, the majority were aged between 47-61 years (31.6%), female (52.3%), with monthly income between 10,000-15,000 Baht (57%), and had a history of alcohol drinking (59.3%). Patient symptoms were abdominal pain (48.6%), followed by iron deficiency anemia (35.3%). Papaya salad consumption (40.3%) was a possible risk factor for H. pylori infection. The prevalence of H. pylori strains resistant to clarithromycin was 76.2%. Among clarithromycin-resistant strains tested, all were due to the A2144G point mutation in the 23S rRNA gene. Among mutations group, wild type genotype, mutant strain mixed wild type and mutant genotype were 23.8%, 35.7% and 40.5% respectively. With the clarithromycin-based triple therapy regimen, the efficacy decreased by 70% for H. pylori eradication (P<0.01). Conclusions: Recent results indicate a high rate of H. pylori resistance to clarithromycin. Mixed of wild type and mutant genotype is the most common mutant genotype in Nakhon Ratchasima province, therefore the use of clarithromycin-based triple therapy an not advisable as an empiric first-line regimen for H. pylori eradication in northeast region of Thailand.

• 한국미생물·생명공학회지
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• 제50권2호
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• pp.301-309
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• 2022

본 연구에서는 제럼본에 처리에 의해 유도된 H. pylori 유전자의 전사적 변화를 분석하였다. NGS를 사용하여 RNA 발현 변화를 분석한 다음 그 결과를 검증하기 위해 RT-PCR을 수행하였다. NGS 분석 결과, 1,632개의 유전자 중 총 23개가 제럼본 처리에 의해 유의하게 발현이 변화된 특이발현 유전자로 분석되었다. DNA 복제와 전사, 병원성 인자 및 T4SS 성분과 관련된 유전자 중 10개는 현저하게 하향 조절되었고 5개는 상향 조절되었다. RT-PCR을 이용하여 유전자의 발현 수준을 재확인하였고 그 결과, 14개 유전자에서 NGS와 동일하게 발현 양상이 변화하였다. RT-PCR은 제럼본 처리에 의해 10개의 유전자(dnaE, dnaQ, rpoA, rpoD, secA, flgE, flhA, virB5, virB8, virB9)의 발현 감소와 4개의 유전자(flaA, flaB, virB4, virD4)의 발현 증가를 보였다. 이러한 본 연구의 결과는 제럼본이 다양한 H. pylori의 병원성과 관련된 인자들을 조절함으로써 H. pylori 감염의 잠재적인 치료제가 될 수 있음을 시사한다.

• 생명과학회지
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• 제26권10호
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• pp.1214-1217
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• 2016

Rebamipoide는 위궤양과 위염치료에 쓰이는 위보호제로 임상에서 사용되고 있지만 위암에서의 역할에 대해서는 알려지바가 거의 없다. 헬리코박토 파일로리(Helicobacter pylori)의 주요독성인자인 CagA는 위암의 발생과 관련이 있다. CagA는 위암세포에서 NFκB의 활성을 증가시켜 PLD1 단백질의 발현을 증가시킴으로써 위암세포의 증식과 침윤을 유도한다. Rebamipide는 NFκB의 활성을 억제함으로써 H. pylori의 CagA에 의해 유도되는 PLD1의 발현을 저해하는것으로 규명되었다. 게다가, rebamipide는 H. pylori의 CagA에 의해 유도되는 β-catenin과 그 표적 유전자로서 인 암줄기세포 마커 단백질의 발현을 증가시킴으로써 위암줄기세포의 자가재생능력을 감소시킨다. 또한 rebamipide는 항암제 내성을 극복하는 화학감수성을 증가시켜서 위암생성을 감소시키는 것으로 나타났다. 그래서 rebamipide는 위암치료제로서의 잠재적 효능을 가지고 있는 약물로서의 가능성이 제시되고 있다.

• 대한수의학회지
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• 제44권4호
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• pp.607-613
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• 2004

Helicobacter pylori (H. pylori)-infection is an important pathogen of stomach cancer after chronic gastritis and ulceration in the stomach and duodenum. However, the virulences of H. pylori strains have not been well-defined between clinical isolates. This study was designed to establish water-immersion-restraint stress (WIRS) model in mongolian gerbil for comparison of pathogenicity of H. pylori strains. To determine an optimal duration time for WIRS model in gerbil, 5-week-old Mongolian gerbils were divided into different groups by WIRS duration time. After graded duration of WIRS, the macroscopic ulcer index (UI) was measured with the stomach and duodenum of sacrificed animal. There were no significant differences between male and female in same duration group. However, the UI increased significantly in a time-dependent fashion. The group of 6 hours-WIRS animals showed severe hemorrhage and ulceration in their stomach and duodenum. On the other hand, the very mild lesions induced in 2 hours-treated animals. Therefore, we determined an optimal duration time for WIRS model in gerbil as 4 hours. Thereafter, we evaluated whether this WIRS model in gerbil could be used as an useful tool for in vivo comparison of pathogenicity of H. pylori strains by enhancement of pathological severity in H. pylori-infected gerbils. Mongolian gerbils were divided into H. pyloriinfected and PBS-inoculated groups. Thereafter, they were divided again into 4 hours-WIRS and no WIRS subgroups. After treatment, the severity of pathological changes was evaluated in a same manner with previous duration-determining experiment. When the animals were exposed to WIRS, the UI was significantly higher in the infected group than in the uninfected group. These results suggested that the established gerbil-WIRS model in this study enhanced effectively the severity of pathogenic changes in the H. pylori-infected Mongolian gerbils and could be used as an useful tool for in vivo comparison of pathogenicity of H. pylori strains.

• 대한의생명과학회지
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• 제26권4호
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• pp.288-295
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• 2020

Infection of Helicobacter pylori on gastric mucosa is associated with various gastric diseases. According to the WHO, H. pylori causes gastric cancer and has been classified as a class I carcinogen. Riboflavin is an essential vitamin which presents in a wide variety of foods. Previous studies have shown that riboflavin/UVA was effective against the growth inhibition of Staphylococcus aureus, S. epidermidis and multidrug-resistant Pseudomonas aeruginosa and had the potential for antimicrobial properties. Thus, we hypothesized that riboflavin has a potential role in the growth inhibition of H. pylori. To demonstrate inhibitory concentration of riboflavin against H. pylori, we performed agar and broth dilution methods. As a result, we found that riboflavin inhibited the growth of H. pylori. The MIC was 1 mM in agar and broth dilution test. Furthermore, to explain the inhibitory mechanism, we investigated whether riboflavin has an influence on the replication-associated molecules of the bacteria using RT-PCR to detect mRNA expression level in H. pylori. Riboflavin treatment of H. pylori led to down-regulation of polA and dnaB mRNA expression levels in a dose dependent manner. After then, we also confirmed whether riboflavin has cytotoxicity to human cells. We used AGS, a gastric cancer cell line, and treated with riboflavin did not show statistically significant decrease of cell viability. Thus, these results indicate that riboflavin can suppress the replication machinery of H. pylori. Taken together, these findings demonstrate that riboflavin inhibits growth of H. pylori by inhibiting replication of the bacteria.

• 한국축산식품학회지
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• 제43권5호
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• pp.751-766
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• 2023

Helicobacter pylori is a bacterium that naturally thrives in acidic environments and has the potential to induce various gastrointestinal disorders in humans. The antibiotic therapy utilized for treating H. pylori can lead to undesired side effects, such as dysbiosis in the gut microbiota. The objective of our study was to explore the potential antibacterial effects of nisin and lactic acid (LA) in yogurt against H. pylori. Additionally, we investigated the anti-inflammatory effects of nisin and LA in human gastric (AGS) cells infected with H. pylori. Nisin and LA combination showed the strongest inhibitory activity, with confirmed synergy at 0.375 fractional inhibitory concentration index. Also, post-fermented yogurt with incorporation of nisin exhibited antibacterial effect against H. pylori. The combination of nisin and LA resulted in a significant reduction of mRNA levels of bacterial toxins of H. pylori and pro-inflammatory cytokines in AGS cells infected with H. pylori. Furthermore, this also increased bacterial membrane damage, which led to DNA and protein leakage in H. pylori. Overall, the combination of nisin and LA shows promise as an alternative therapy for H. pylori infection. Additionally, the incorporation of nisin into foods containing LA presents a potential application. Further studies, including animal research, are needed to validate these findings and explore clinical applications.

• 미생물학회지
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• 제48권2호
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• pp.109-115
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• 2012

Helicobacter pylori는 만성 위염, 소화성 궤양, 위암의 중요한 역학적 인자중 하나이다. H. pylori의 독성인자중 CagL은 숙주 세포와 H. pylori의 제 4형 분비기관(Type 4 secretion system)을 연결하는 adhesin으로 작용하는 섬모 단백질로 H. pylori가 발병하는데 중요한 역할을 하는 것으로 알려져 있다. 이번 연구는 저빌에 H. pylori를 감염시킨 동물 모델을 이용하여 CagL 재조합 단백질을 면역화시켰을 때 나타나는 효과를 평가하였다. 재조합 CagL은 클론되었고, 과발현시켜 정제하여 준비하였다 저빌은 H. pylori 감염 대조군과 H. pylori 감염 CagL 재조합 단백질 접종군으로 분류하였고, 접종시 알루미늄 애쥬번트를 사용하였다. 일주일 간격으로 4회 근육내 접종하였고, 마지막 접종 일주일 후, 모든 저빌에 H. pylori 7.13 균주를 $1{\times}10^9\;bacteria/500{\mu}l$ 농도로 위내 투여하였다. H. pylori 감염 6주째 모든 저빌을 희생하여 혈청 IgG 반응평가를 위한 ELISA를 실시하였고, 위에서는 집락화된 H. pylori의 수평가, 병리조직학적 평가 및 사이토카인 유전자발현을 조사하였다. CagL 재조합 단백질접종 일주일 후부터 H. pylori 감염 CagL 재조합 단백질 접종군의 혈청내 IgG 항체형성이 유의적으로 증가하였다. 위에서의 집락화된 세균수는 두군의 차이가 없었다. 저빌 체중에 대한 위무게 비율는 H. pylori 감염 CagL 재조합 단백질 접종군이 유의적으로 감소하였으나 병리조직학적 평가에서는 유의적인 차이는 확인하지 못하였다. 위에서의 IL-$1{\beta}$와 KC (IL-8 homologues)의 유전자발현 정도도 두 군사이에 유의적인 차이는 없었다. 이번 결과는 CagL 재조합 단백질의 접종은 IgG 항체형성은 효과적으로 자극하였지만 면역화된 숙주에서 세균 집락화의 감소 및 병변형성의 방어까지는 유도하지 못한 것으로 나타났으며, 앞으로 H. pylori 감염에 대해 유효한 면역 반응 및 질병 방어 효과를 나타내기 위해서 CagL을 포함한 다른 종류의 재조합 항원 사용 및 보조적으로 전신 면역 및 점막 면역을 효과적으로 유도하기 위해 안정성있는 애쥬번트의 사용을 고려해야 할 것으로 사료된다.

• 대한한방내과학회지
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• 제33권1호
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• pp.39-53
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• 2012

Objectives : Many studies have shown that helicobacter pylori (H. pylori) infection is associated with gastroduodenal diseases. The purpose of this report was to evaluate recently published research on the influence of oriental herbal medicine on H. pylori infections. Methods : Recently published literature were systematically compared with their findings of how oriental herbal medical treatment affects H. pylori-associated disease. Results : The eradication rate of H. pylori in oriental herbal medicine groups was 66.93% while it was 66.02% in western medicine groups. In oriental herbal plus western medicine groups, interestingly, the rate increased to 84.78%. On the other hand, the total treatment efficacy rate of H. pylori in oriental herbal medicine groups was 91.27%. The treatment efficacy rate in oriental herbal plus western medicine groups rose to a record 93.22%, which was 15.34% higher than the rate in western medicine groups. In addition, the rate of adverse effects was 2.71%, 4.85%, 15.80% in oriental herbal medicine, western medicine, and oriental herbal plus western medicine groups, respectively. Diarrhea was most frequently observed in oriental herbal medicine groups, while nausea was most frequently observed in the other groups. Conclusions : The results of this study showed that herbal medicinal treatment can increase the rate of H. pylori eradication and improve H. pylori-related gastrointestinal symptoms. These findings suggest that herbal medicine can solve the problems including side effects due to antibiotic resistance of standard triple therapy.

• 대한미생물학회지
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• 제34권6호
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• pp.519-532
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• 1999

Helicobacter pylori is a causative agent of type B gastritis and plays a central role in the pathogenesis of gastroduodenal ulcer and gastric cancer. To elucidate the host-parasite relationship of the H. pylori infection on the basis of molecular biology, we tried to evaluate the genomic diversity of H. pylori. An ordered overlapping bacterial artificial chromosome (BAC) library of a Korean isolate, H. pylori 51 was constructed to set up a genomic map. A circular physical map was constructed by aligning ApaI, NotI and SfiI-digested chromosomal DNA. When the physical map of H. pylori 51 was compared to that of unrelated strain, H. pylori 26695, completely different restriction patterns were shown. Fifteen known genes were mapped on the chromosome of H. pylori 51 and the genetic map was compared with those of strain 26695 and J99, of which the entire genomic sequences were reported. There were some variability in the gene location as well as gene order among three strains. For further analysis on the genomic diversity of H. pylori, when comparing the genomic structure of 150 H. pylori Korean isolates with one another, genomic macrodiversity of H. pylori was characterized by several features: whether or not susceptible to restriction digestion of the chromsome, variation in chromosomal restriction fingerprint and/or high frequency of gene rearrangement. We also examined the extent of allelic variation in nucleotide or deduced amino acid sequences at the individual gene level. fucT, cagA and vacA were confirmed to carry regions of high variation in nucleotide sequence among strains. The plasticity zone and strain-specific genes of H. pylori 51 were analyzed and compared with the former two genomic sequences. It should be noted that the H. pylori 51-specific sequences were dispersed on the chromosome, not congregated in the plasticity zone unlike J99- or 26695-specific genes, suggesting the high frequency of gene rearrangement in H. pylori genome. The genome of H. pylori 51 shows differences in the overall genomic organization, gene order, and even in the nucleotide sequences among the H. pylori strains, which are far greater than the differences reported on the genomic diversity of H. pylori.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제23권3호
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• pp.243-250
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• 2020

Purpose: Gastric delta cells (D-cells), which are somatostatin-secreting cells, are the main paracrine inhibitor of acid secretion. The number of D-cells was studied in children presenting with upper gastrointestinal (UGI) disease. Methods: We retrospectively investigated the number of D-cells in the gastric body and antrum through immunofluorescence examinations according to symptoms, endoscopic findings, and Helicobacter pylori infection in 75 children who visited Hanyang University Hospital Pediatrics. Results: The mean patient age was 12.2±3.3 years. The male-to-female ratio was 1:1.4. The mean D-cell number per high-power field in the antrum and body was 20.5 and 12 in children with substernal pain, 18.3 and 10.3 in vomiting, 22.3 and 6 in diarrhea, and 9.3 and 6 in abdominal pain, respectively (p>0.05). According to endoscopic findings, the mean D-cell number in the antrum and body was 14.3 and 6 with gastritis, 14 and 9.3 with reflux esophagitis, 16.7 and 8.7 with duodeno-gastric reflux, 19.3 and 12.7 with gastric ulcer, 16 and 13.7 with duodenitis, and 12.3 and 4 with duodenal ulcer, respectively (p>0.05). The D-cell number in the gastric body was 2.7 and 8.7 in children with current H. pylori infection and non-infected children, respectively (p=0.01), while those in the antrum were 15.5 and 14, respectively, with no statistical significance. Conclusion: The D-cell number was lower in the gastric body of children with current H. pylori infection. Further studies concerning peptide-secreting cells with a control group would provide information about the pathogenic pathways of UGI disorder.