scholarly journals Long-Term Use of Probiotic-Containing Yogurts Is a Safe Way to PreventHelicobacter pylori: Based on a Mongolian Gerbil's Model

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Chao-Hung Kuo ◽  
Sophie S. W. Wang ◽  
Chien-Yu Lu ◽  
Huang-Ming Hu ◽  
Fu-Chen Kuo ◽  
...  

Background. The suppression ofHelicobacter pylori(H. pylori) decreasesH. pylori-related diseases. The probiotics have an inhibitory effect onH. pylori.Aim. We investigated the effects of long-term use of yogurt onH. pyloribased on Mongolian gerbils’ model.Materials and Methods. Yogurt (containing a supplement ofLactobacillus acidophilus, Bifidobacterium lactis, etc.) was used. Forty-six gerbils were divided into five groups. All groups were inoculated withH. pylorifor 5 to 8 weeks. The yogurt was given as follows: Group (Gr.) A: from 1st to 4th week; Gr. B from 5th to 8th week; Gr. C: from 17th week to sacrifice; Gr. D: from 5th week to sacrifice. Gerbils were sacrificed on the 52nd week. Histology was evaluated according to the Sydney system.Results. The positive rates ofH. pyloriwere 60% (Gr. A), 75% (Gr. B), 67% (Gr. C), 44% (Gr. D), and 100% (Gr. E). Gr. D showed lower inflammatory score. Only Gr. E (60%) had intestinal metaplasia. Gr. D showed higher IL-10 and lower TNF-αexpression than Gr. E.Conclusion.Long-term intake of yogurt could decreaseH. pyloriinfection. The long-term use of yogurt would be an alternative strategy to manageH. pyloriinfection.

2000 ◽  
Vol 192 (11) ◽  
pp. 1601-1610 ◽  
Author(s):  
Keiji Ogura ◽  
Shin Maeda ◽  
Masafumi Nakao ◽  
Takeshi Watanabe ◽  
Mayumi Tada ◽  
...  

Helicobacter pylori infection induces various gastroduodenal diseases. We examined the role of two genes, vacA and cagE, in the gastric pathogenesis induced by H. pylori using a long-term (62 wk) animal model. Reportedly, both genes are associated with the virulence of H. pylori: vacA encodes vacuolating cytotoxin, and cagE, with other genes in the cag pathogenicity islands, encodes a type IV secretion system. Mongolian gerbils were challenged in this study by a wild-type TN2 strain and its isogenic mutants of cagE or vacA. The wild-type and vacA mutants induced severe gastritis, whereas cagE mutants induced far milder changes. Gastric ulcer was induced at the highest rate (22/23) by the wild-type TN2, followed by the vacA mutant (19/28). No ulcer was found in the gerbils infected with the cagE mutant (0/27) or in controls (0/27). Intestinal metaplasia was also found in the gerbils infected with the wild-type (14/23) or vacA mutant (15/28). Gastric cancer developed in one gerbil with wild-type infection and in one with vacA mutant infection. In conclusion, the knocking out of the cagE gene deprived wild-type H. pylori of the pathogenicity for gastritis and gastric ulcer, suggesting that the secretion system encoded by cag pathogenicity island genes plays an essential role.


2014 ◽  
Vol 63 (1) ◽  
pp. 129-137 ◽  
Author(s):  
Cynthia Zaman ◽  
Takako Osaki ◽  
Tomoko Hanawa ◽  
Hideo Yonezawa ◽  
Satoshi Kurata ◽  
...  

Animal models are essential for in vivo analysis of Helicobacter-related diseases. Mongolian gerbils are used frequently to study Helicobacter pylori-induced gastritis and its consequences. The presence of some gastric microbiota with a suppressive effect on H. pylori suggests inhibitory gastric bacteria against H. pylori infection. The aim of the present study was to analyse the microbial ecology between H. pylori and the gastric microbiota of Mongolian gerbils. Gastric mucosa samples of H. pylori-negative and -positive gerbils were orally inoculated to five (Group 1) and six (Group 2) gerbils, respectively, and the gerbils were challenged with H. pylori infection. The colonization rate (40 %) of H. pylori in Group 1 gerbils was lower than the rate (67 %) in Group 2 gerbils. Culture filtrate of the gastric mucosa samples of Group 1 gerbils inhibited the in vitro growth of H. pylori. Three lactobacilli species, Lactobacillus reuteri, Lactobacillus johnsonii and Lactobacillus murinus, were isolated by anaerobic culture from the gerbils in Groups 1 and 2, and identified by genomic sequencing. It was demonstrated that the three different strains of lactobacilli exhibited an inhibitory effect on the in vitro growth of H. pylori. The results suggested that lactobacilli are the dominant gastric microbiota of Mongolian gerbils and the three lactobacilli isolated from the gastric mucosa samples with an inhibitory effect on H. pylori might have an anti-infective effect against H. pylori.


2005 ◽  
Vol 12 (2) ◽  
pp. 347-353 ◽  
Author(s):  
Shigehito Nakagawa ◽  
Takako Osaki ◽  
Yasunori Fujioka ◽  
Hiroyuki Yamaguchi ◽  
Shigeru Kamiya

ABSTRACT The effects of long-term infection with Helicobacter pylori on the gastric mucosa of Mongolian gerbils were examined. Colonization by H. pylori was evaluated by both microaerobic cultivation and real-time reverse transcriptase PCR (RT-PCR). Persistent infection with H. pylori in gastric mucosa was detected by real-time RT-PCR during 6 months after infection, but no H. pylori was isolated 4 months after infection by cultivation. Infiltration with neutrophils and mononuclear cells was observed from 2 months after infection. Both intestinal metaplasia and gastric atrophy were also detected from 2 months after infection. The results by enzyme-linked immunosorbent assay indicated that antibody titers against whole H. pylori antigens, H. pylori heat shock protein 60 (HSP60), and Escherichia coli GroEL were significantly higher in the infected gerbils than in noninfected gerbils. After long-term infection with H. pylori for 18 months, marked atrophy of gastric mucosa and multiple cysts in the submucosa were observed in the glandular stomach of the infected gerbils. In addition, squamous cell papilloma with hyperkeratosis was observed in cardia of all the infected gerbils. These results indicate that evaluation of bacterial colonization during long-term infection can be done by real-time RT-PCR and that mucosal damage might be induced by host immune response against whole H. pylori antigen.


2017 ◽  
Vol 4 (S) ◽  
pp. 46
Author(s):  
Truong Xuan Bui

Gastric cancer is one of the leading cancer lesions in Vietnam. Up to now, Helicobacter pylori (H. pylori) infection is still remaining a major pathogenic factor in patients with peptic disorders in Vietnam. Aims: The aim of the study was evaluated the correlation between H. pylori infection with atrophic gastritis (AG), intestinal metaplasia (IM) and dysplasia (DP) in gastritis Vietnamese. Patients and Methods: A total of 161 gastritis patients including 105 males and 56 females with mean of age of 49.81 ± 11.32 years (21 - 79 years) were enrolled in the study. Upper GI endoscopy was evaluated in all patients and afterward gastric biopsy specimens were taken according to the recommendation of update Sydney system and modified Baylor. The gastric biopsy specimens were analyzed with skilled pathologist who did not know about clinico-endoscopic status. The confirmation of H. pylori infection was evaluated with urease test (clo-test) and Giemsa staining. Results: Of the 161 patients, 96 (59.6%) patients were infected with H. pylori, and about 72.05% (116/161) of patients was suffered from atrophic gastritis. The prevalence of atrophic gastritis in H. pylori infected patients (83/96, 86.45%) was significantly higher than that in non-infected patients (33/65, 50.76%), p = 0.041. In the study, the prevalence of intestinal metaplasia and dysplasia was 84/161 (52.17%) and 17/161 (10.55%), respectively. The prevalence of intestinal metaplasia in H. pylori infected patients was observed significantly higher than that in non-infected patients (61/96, 63.54% vs. 23/65, 35.38%, p = 0.044); and the prevalence of dysplasia in H. pylori infected patients was also higher than that in non-infected patients (14/96, 14.58% vs. 3/65, 4.61%, p = 0.073). Conclusion: In gastritis Vietnamese, H. pylori was related to atrophic gastritis, intestinal metaplasia and dysplasia, so gastritis Vietnamese infected with H. pylori could be categorized into high risk group for screening gastric cancer.


2014 ◽  
Vol 2014 ◽  
pp. 1-7
Author(s):  
Chao-Hung Kuo ◽  
Chien-Yu Lu ◽  
Yuan-Chieh Yang ◽  
Chieh Chin ◽  
Bi-Chuang Weng ◽  
...  

Background. It is urgent to find alternative agents due to increasing failure rate ofHelicobacter pylori (H. pylori) eradication. The study surveyed the long-term effect of silver nanoparticles (AgNP) onH. pyloribased on Mongolian gerbil’s model.Materials and Methods. Fifty gerbils were randomly allocated to six groups (A–F). Group (Gr) A: the gerbils were fed with broth; Gr B and D: the gerbils were fed with AgNP/clay complex (0.1% of weight); Gr C and E: the gerbils were fed with AgNP/clay complex(1% of weight); and Gr D, E, and F: the gerbils were inoculated withH. pylori. At the 20th experimental week, the gerbils were sacrificed. Histology was evaluated according to the classification of the Sydney system.P<0.05was considered to be statistically significant.Results. The AgNP/clay has more obvious inhibitory effect onH. pyloriin vitro. There was a trend of higher concentrations of AgNP with stronger inhibitory effect onH. pylorigrowth(P=0.071). There were no significant differences of inflammation among groups D, E, and F(P=0.688).Conclusion. AgNP/clay would be a potential and safe agent for inhibitingH. pylori. It should be helpful for eradication ofH. pyloriinfection.


2021 ◽  
Vol 22 (5) ◽  
pp. 2695
Author(s):  
Paweł Krzyżek ◽  
Paweł Migdał ◽  
Emil Paluch ◽  
Magdalena Karwańska ◽  
Alina Wieliczko ◽  
...  

Helicobacter pylori, a gastric pathogen associated with a broad range of stomach diseases, has a high tendency to become resistant to antibiotics. One of the most important factors related to therapeutic failures is its ability to change from a spiral to a coccoid form. Therefore, the main aim of our original article was to determine the influence of myricetin, a natural compound with an antivirulence action, on the morphological transformation of H. pylori and check the potential of myricetin to increase the activity of antibiotics against this pathogen. We observed that sub-minimal inhibitory concentrations (sub-MICs) of this compound have the ability to slow down the process of transformation into coccoid forms and reduce biofilm formation of this bacterium. Using checkerboard assays, we noticed that the exposure of H. pylori to sub-MICs of myricetin enabled a 4–16-fold reduction in MICs of all classically used antibiotics (amoxicillin, clarithromycin, tetracycline, metronidazole, and levofloxacin). Additionally, RT-qPCR studies of genes related to the H. pylori morphogenesis showed a decrease in their expression during exposure to myricetin. This inhibitory effect was more strongly seen for genes involved in the muropeptide monomers shortening (csd3, csd6, csd4, and amiA), suggesting their significant participation in the spiral-to-coccoid transition. To our knowledge, this is the first research showing the ability of any compound to synergistically interact with all five antibiotics against H. pylori and the first one showing the capacity of a natural substance to interfere with the morphological transition of H. pylori from spiral to coccoid forms.


2000 ◽  
Vol 118 (4) ◽  
pp. A1302-A1303
Author(s):  
Kiichi Satoh ◽  
Ken Kihira ◽  
Hiroshi Kawata ◽  
Keiko Fukazawa ◽  
Satoshi Kawakami ◽  
...  

2014 ◽  
Vol 70 ◽  
pp. 107-113 ◽  
Author(s):  
Takanori Yamada ◽  
Min Wei ◽  
Takeshi Toyoda ◽  
Shoutaro Yamano ◽  
Hideki Wanibuchi

2018 ◽  
Vol 11 (3) ◽  
pp. 187-193 ◽  
Author(s):  
Petruta Violeta Filip ◽  
◽  
Denisa Cuciureanu ◽  
Laura Sorina Diaconu ◽  
Ana Maria Vladareanu ◽  
...  

Primary gastric lymphoma (PGL) represents a rare pathology, which can be easily misdiagnosed because of unspecific symptoms of the digestive tract. Histologically, PGL can vary from indolent marginal zone B-cell lymphoma of the mucosa-associated lymphoid tissue (MALT) to aggressive diffuse large B-cell lymphoma (DLBCL). During the years, clinical trials revealed the important role of Helicobacter pylori (H. pylori) in the pathogenesis of gastric MALT lymphoma. Infection with Helicobacter pylori is an influential promoter of gastric lymphomagenesis initiation. Long-term studies revealed that eradication therapy could regress gastric lymphomas.


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