Significance of dormant forms of<i>Helicobacter pylori</i>in ulcerogenesis

Reshetnyak, Vasiliy Ivanovich; Reshetnyak, T.

doi:10.3748/wjg.v23.i27.4867

Cited by 68 publications

(53 citation statements)

References 101 publications

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“…Previous authors have referred to these forms as the C-shaped and U-shaped forms and they are the precursors to the coccoid form. These C-shaped and U-shaped forms of H. pylori are considered to be bacterial intermediates that favor survival transforming them into an inactive phase (dormancy) [28,29], due to adverse condition, as temperature or pH changes, use of antimicrobial drugs, prolonged fasting when cultivated, deficiency of nutrients, effects of antisecretory drugs, etc. [30].…”

Section: Discussionmentioning

confidence: 99%

High expression of Helicobacter pylori VapD in both the intracellular environment and biopsies from gastric patients with severity

et al. 2020

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Helicobacter pylori is a Gram-negative bacterium that causes chronic atrophic gastritis and peptic ulcers and it has been associated with the development of gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT). One of the more remarkable characteristics of H. pylori is its ability to survive in the hostile environment of the stomach. H. pylori regulates the expression of specific sets of genes allowing it to survive high acidity levels and nutrient scarcity. In the present study, we determined the expression of virulence associated protein D (VapD) of H. pylori inside adenocarcinoma gastric (AGS) cells and in gastric biopsies. Using qRT-PCR, VapD expression was quantified in intracellular H. pylori-AGS cell cultures at different time points and in gastric mucosa biopsies from patients suffering from chronic atrophic gastritis, follicular gastritis, peptic ulcers, gastritis precancerous intestinal metaplasia and adenocarcinoma. Our results show that vapD of H. pylori presented high transcription levels inside AGS cells, which increased up to two-fold above basal values across all assays over time. Inside AGS cells, H. pylori acquired a coccoid form that is metabolically active in expressing VapD as a protection mechanism, thereby maintaining its permanence in a viable non-cultivable state. VapD of H. pylori was expressed in all gastric biopsies, however, higher expression levels (p = 0.029) were observed in gastric antrum biopsies from patients with follicular gastritis. The highest VapD expression levels were found in both antrum and corpus gastric biopsies from older patients (>57 years old). We observed that VapD in H. pylori is a protein that is only produced in response to interactions with eukaryotic cells. Our results suggest that VapD contributes to the persistence of H. pylori inside the gastric epithelial cells, protecting the microorganism from the intracellular environment, reducing its growth rate, enabling long-term infection and treatment resistance. PLOS ONEPLOS ONE | https://doi.org/10.1371/journal.pone.et al. (2020) High expression of Helicobacter pylori VapD in both the intracellular environment and biopsies from gastric patients with severity. PLoS ONE 15(3): e0230220. https://doi.org/10.

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Section: Discussionmentioning

confidence: 99%

High expression of Helicobacter pylori VapD in both the intracellular environment and biopsies from gastric patients with severity

et al. 2020

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“…Among them, the coccoid form is divided into two subtypes. Type A has irregular edges with a rough surface and is considered to be a dead form, while type B has a smoother surface, is smaller and is considered to be a dormant form . A previous study has confirmed that coccoid H pylori exists in the stomach and duodenum, and the number in the duodenum is higher than that in the stomach.…”

Section: Influencing Factors Of H Pylori Recrudescencementioning

confidence: 96%

Helicobacter pylori recrudescence and its influencing factors

Sun

Zhang

2019

J Cellular Molecular Medi

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Helicobacter pylori (H pylori) is known as one of the most common infectious pathogens, with high infection and recurrence rates worldwide. The prevalence of H pylori is up to 90% in developing countries, while the annual recurrence rate is much higher than that in developed countries. Recurrence can occur either by recrudescence or reinfection. Compared with reinfection, the time window for recrudescence is generally shorter, followed by the recurrence of H pylori–associated diseases in the short‐term. Many factors are involved in the H pylori reinfection, such as the prevalence of H pylori infection, living conditions and economic development, health conditions and so forth. Previous studies focused less on H pylori recrudescence. Therefore, the influencing factors for H pylori recrudescence needed further exploration. This study reviewed the recrudescence of H pylori infection and its influencing factors.

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“…The bacterium is, indeed, known to be able to resist harsh environments by changing to a dormant, inactive state, a non-culturable coccoid form that could still be potentially viable, later on, in the stomach (21,22) . It is therefore possible that H. pylori may lay dormant for long periods of time, using the nose and the sinuses as reservoirs, waiting for an eventual return to an active form, either to cause gastric re-infection or to participate in the oral-oral route of transmission.…”

Section: Resultsmentioning

confidence: 99%

Helicobacter pylori in both the sinuses and the stomach

Dinis¹,

Matos²,

Sardinha³

et al. 2018

RHINOL

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Background: The role played by Helicobacter pylori in the sinuses, and its association with the same organism's gastric infection, are still unclear. Methods: In order to compare H.pylori colonization patterns in the nose and stomach we conducted a cohort analysis of 14 patients, eligible for sinus surgery due to chronic medically refractory rhinosinusitis, who were tested for simultaneous presence of H. pylori, by histology, culture and polymerase chain reaction, in pathologic sinus tissue collected during surgery and in gastric mucosa obtained through gastroduodenal endoscopy. Results: H. pylori DNA was found in the sinus mucosa of 15.4% of patients with chronic rhinosinusitis, and all of them showed concurrent H. pylori stomach infection. Sinus colonization was not found without simultaneous gastric colonization, although most patients with gastric infection did not have the bacterial DNA in their sinuses. H. pylori's presence in the nose was not associated with local inflammatory status, and no cultures could be obtained from any of the sinus tissue samples, including those positive for H. pylori DNA. Conclusions: Only H. pylori DNA, and not the culturable active form of the microorganism, could be found in the sinus mucosa of some patients with H. pylori gastric infection. We could not find evidence, however, that the bacterium's presence in the nose contributes to local mucosal inflammation.

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Significance of dormant forms ofHelicobacter pyloriin ulcerogenesis

Cited by 68 publications

References 101 publications

High expression of Helicobacter pylori VapD in both the intracellular environment and biopsies from gastric patients with severity

High expression of Helicobacter pylori VapD in both the intracellular environment and biopsies from gastric patients with severity

Helicobacter pylori recrudescence and its influencing factors

Helicobacter pylori in both the sinuses and the stomach

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