Virulence of water-induced coccoid<i>Helicobacter pylori</i>and its experimental infection in mice

She, Feifei; Lin, Jianqun; Liu, Junyan; Huang, Chien-Chang; Su, Donghui

doi:10.3748/wjg.v9.i3.516

Cited by 64 publications

(66 citation statements)

References 31 publications

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“…As H. pylori is a human pathogen, it is possible that the VBNC form is more infectious in humans than in mice. Further, we only exposed mice to one strain of H. pylori , and it is possible that other strains would be more infectious in the VBNC state than SS1, as has been seen in other published papers in the literature 19, 27. Despite our large sample sizes and high doses, our inability to infect mice with VBNC H. pylori via drinking water suggests that VBNC SS1 in water is not infectious in mice.…”

Section: Discussionmentioning

confidence: 95%

“…She et al 19. found that 11 of 16 mice gavaged with VBNC H. pylori were infected compared to 14 of 16 gavaged with the same dose of viable, culturable H. pylori .…”

Section: Discussionmentioning

confidence: 99%

“…We performed four mouse experiments to assess the infectivity of VBNC H. pylori in various different exposure scenarios (Table 1). Concentrations of VBNC H. pylori were chosen based on previous studies19, 20, 23 and on the amounts of H. pylori found in sources of recreational and drinking water worldwide 24, 25. We first employed a classic single‐hit exposure model with waterborne VBNC H. pylori , examining whether a single day of water with a high dose of H. pylori could cause infection, choosing the high end of waterborne concentrations to test a “worst‐case” scenario and to try to ensure a higher chance of experimental infection; 4 weeks was chosen as the time to wait until euthanasia, given that She et al 19.…”

Section: Methodsmentioning

confidence: 99%

“…She et al 19. inoculated sterilized tap water with live H. pylori and stored it at 4°C for 40 days, defining cells as VBNC when they were in the coccoid state and did not grow when plated.…”

Section: Methodsmentioning

confidence: 99%

“…Furthermore, H. pylori has been detected in water using various molecular biology techniques, such as quantitative polymerase chain reaction (qPCR) and microscopy methods,5, 10, 11, 12, 13 and there are reports that it has been cultured from water 14, 15, 16, 1718, 19, 20. This change is often accompanied by a morphological change from a spiral bacillus to a U‐shaped or coccoid form, and H. pylori has been found in the VBNC state in all these morphologies in the natural environment 18, 21.…”

Section: Introductionmentioning

confidence: 99%

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Reduced infectivity of waterborne viable but nonculturable Helicobacter pylori strain SS1 in mice

et al. 2017

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Background Helicobacter pylori infection has been consistently associated with lack of access to clean water and proper sanitation, but no studies have demonstrated that the transmission of viable but nonculturable (VBNC) H. pylori can occur from drinking contaminated water. In this study, we used a laboratory mouse model to test whether waterborne VBNC H. pylori could cause gastric infection.Materials and MethodsWe performed five mouse experiments to assess the infectivity of VBNC H. pylori in various exposure scenarios. VBNC viability was examined using Live/Dead staining and Biolog phenotype metabolism arrays. High doses of VBNC H. pylori in water were chosen to test the “worst‐case” scenario for different periods of time. One experiment also investigated the infectious capabilities of VBNC SS1 using gavage. Further, immunocompromised mice were exposed to examine infectivity among potentially vulnerable groups. After exposure, mice were euthanized and their stomachs were examined for H. pylori infection using culture and PCR methodology.Results VBNC cells were membrane intact and retained metabolic activity. Mice exposed to VBNC H. pylori via drinking water and gavage were not infected, despite the various exposure scenarios (immunocompromised, high doses) that might have permitted infection with VBNC H. pylori. The positive controls exposed to viable, culturable H. pylori did become infected.ConclusionsWhile other studies that have used viable, culturable SS1 via gavage or drinking water exposures to successfully infect mice, in our study, waterborne VBNC SS1 failed to colonize mice under all test conditions. Future studies could examine different H. pylori strains in similar exposure scenarios to compare the relative infectivity of the VBNC vs the viable, culturable state, which would help inform future risk assessments of H. pylori in water.

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Section: Discussionmentioning

confidence: 95%

“…She et al 19. found that 11 of 16 mice gavaged with VBNC H. pylori were infected compared to 14 of 16 gavaged with the same dose of viable, culturable H. pylori .…”

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Reduced infectivity of waterborne viable but nonculturable Helicobacter pylori strain SS1 in mice

et al. 2017

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Proliferative and apoptotic effects of gastric epithelial cells induced by coccoid Helicobacter pylori

Han

Chen

et al. 2012

J. Basic Microbiol.

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Helicobacter pylori exhibit morphology convertion in a spiral or coccoid form. This study aims to reveal the impact of coccoid H. pylori on the proliferation and apoptosis of gastric epithelial cells. The cagA and vacA genes of H. pylori were detected by semi-quantitative RT-PCR. Proliferation and apoptosis were analyzed by the CCK-8 colorimetric method and TUNEL assay, respectively. Egr-1 mRNA and PCNA expression affected by the ERK1/2-specific inhibitor were detected by RT-PCR and immunochemistry. At low density of infection (MOI < 125:1), coccoid H. pylori exerted a stronger effect on proliferation and a weaker effect on apoptosis than did spiral form. The ERK1/2-specific inhibitor significantly blocked the increased expression in Egr-1 and PCNA induced by coccoid H. pylori. Expression of vacA and cagA in coccoid H. pylori decreased compared with the spiral form, whereas vacA decreased more than cagA. The difference of proliferation and apoptosis may be related to the unequal decreased expression of vacA and cagA in coccoid H. pylori. Activation of the ERK1/2-Egr-1-PCNA signal transduction pathway may play an important role in coccoid H. pylori-induced cell proliferation. Long latency of the coccoid form of H. pylori in gastric tissue may be associated with gastric cancer caused by H. pylori.

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Helicobacter pylori Pathogenesis and Vaccines

Ruggiero

Immunity Against Mucosal Pathogens

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Virulence of water-induced coccoidHelicobacter pyloriand its experimental infection in mice

Cited by 64 publications

References 31 publications

Reduced infectivity of waterborne viable but nonculturable Helicobacter pylori strain SS1 in mice

Reduced infectivity of waterborne viable but nonculturable Helicobacter pylori strain SS1 in mice

Proliferative and apoptotic effects of gastric epithelial cells induced by coccoid Helicobacter pylori

Helicobacter pylori Pathogenesis and Vaccines

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