Helicobacter pylori: recent advances in the study of its pathogenicity and prevention

Aguilar, Germán R.; Ayala, Guadalupe; Fierros-Zarate, Geny

doi:10.1590/s0036-36342001000300010

Cited by 21 publications

(15 citation statements)

References 133 publications

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“…The resistance trait could be spread horizontally by plasmids to other bacterial population. Emergence of a resistance phenotype is a short-term phenomenon that takes 4 – 5 years to emerge and the driving force is the indiscriminate, short-interval and frequent use of antibiotics [33-35]. Clarithromycin resistance rate was high in H. pylori isolates probably contributed to by use of this drug for other indications in the community and this might result in selection of stable macrolide-resistant H.pylori and indigenous microbiota [36].…”

Section: Discussionmentioning

confidence: 99%

Low rate of recurrence of Helicobacter Pylori infection in spite of high clarithromycin resistance in Pakistan

et al. 2013

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BackgroundThe aim was to investigate the reinfection rate of H. pylori during a follow-up period of 12 months in adults who had undergone eradication therapy.MethodsOne hundred-twenty patients; 116 with gastritis, 3 with duodenal ulcer and 1 gastric ulcer, were studied. Their mean age was 41 ± 13 years (range 18–77) and male: female ratio of 2:1. H. pylori were cultured and antibiotic sensitivity was determined by Epsilometer test (E-test) for clarithromycin (CLR) and amoxicillin (AMX). Primers of urease C gene of H. pylori and Sau-3 and Hha I restriction enzymes were used for polymerase chain reaction-restriction fragment length polymorphism analysis (PCR-RFLP). 14C urea breath test (14C-UBT) was performed 4 weeks after the eradication therapy. The successfully treated patients were observed for 12 months with 14C-UBT to assess H. pylori status. If 14C-UBT was negative, it was repeated after every 12 weeks. If 14C-UBT was positive, endoscopy was repeated with biopsies.ResultThe eradication therapy was successful in 102(85%) patients. Out of forty-seven H. pylori isolates cultured, clarithromycin sensitivity was present in 30(64%) and amoxicillin in 45(98%), respectively. Follow-up 14C-urea breath tests of all 102 patients who eradicated H. pylori remained negative up to 9 months. However, in 6 patients, the 14C-UBT confirmed recurrence at 12 months. The recurrence rate was 6%.ConclusionA low rate of recurrence of H. pylori infection was found in patients with dyspeptic symptoms. H. pylori isolates demonstrated a high invitro clarithromycin resistance.

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Section: Discussionmentioning

confidence: 99%

Low rate of recurrence of Helicobacter Pylori infection in spite of high clarithromycin resistance in Pakistan

et al. 2013

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“…Proteins such as alkylhydroperoxide reductase (TsaA) act in an important manner during inflammatory responsegenerated oxidative stress as a defense mechanism, act as neutralizers of reactive oxygen species [4] , or act as chaperones that prevent the denaturalization of certain proteins. In studies performed in AGS cells, the over-expression of IL-8, nitric oxide synthase, and cyclooxigenase-2 was detected [48,49].…”

Section: Discussionmentioning

confidence: 99%

“…Each protein was identified by comparing the sequences obtained by mass spectrometry with the reported peptide sequences. The reported sequences were based on NCBInr data [4] and a global score higher than that established for each peptide was obtained ( Table 1). Some of the identified H. pylori 7C proteins were functionally classified as citosols: flavodoxine (FldA), thiorredoxine (TrxA), the urease alpha subunit (UreA), and the cytotoxin-associated protein or immunodominant antigen (CagA9) ( Table 1).…”

Section: Identified Proteinsmentioning

confidence: 99%

“…It has been suggested that the association between H. pylori and gastric cancer may be attributable to collateral damage produced in gastric epithelial cells due to inflammatory event-induced mutations mediated by reactive oxygen species [4], interleukin (IL)-8, tumor necrosis factor-alpha (TNF-), and IL-1, which are markers for atrophic gastritis, intestinal metaplasia, dysplasia, and carcinoma. On the other hand, gastric adenocarcinoma may be the result of the interaction with H. pylori or of the release of virulence factors such as vacuolize cytotoxin.…”

Section: Introductionmentioning

confidence: 99%

“…Nonetheless, it is known that H. pylori virulence factors such as urease [4,7], lipopolysaccharide [5,8], gammaglutamyltranspeptidase [6], cytotoxin-associated gene protein [9], and vacuolating cytotoxin A [9][10][11] induce apoptosis, and it has been suggested that other factors could participate in the induction of apoptosis. Examining differential H. pylori-protein expression during apoptosis is crucial, as is the study and identification of these proteins that are over-or under-expressed, in order to ascertain their relevance in H. pylori pathogenesis and their clinical effects during infection.…”

Section: Introductionmentioning

confidence: 99%

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Comparative Proteomic Analysis of Helicobacter pylori-Expressed Proteins in Gastric Epithelial Cell Apoptosis (Supplementry Material)

Castillo-Rojas¹,

Adriana²,

Guillermo³

et al. 2009

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Helicobacter pylori infection induces an increase in the rate of apoptosis in gastric epithelial cells and initiates a secondary hyperproliferative response. Currently, cytotoxin-associated proteins and vacuolating cytotoxin participate in the induction of the apoptotic process in the gastric epithelium, however, the existence of other factors that participate in this process has not been ruled out. Moreover, differential protein expression by H. pylori during the apoptotic process has not been studied. The aim of this work was to study differential H. pylori protein expression during the process of apoptosis in AGS cell. AGS cells were infected with H. pylori and apoptosis was determined by measuring chromatin condensation and caspase-3 activity. In addition, bacterial and cellular protein extraction was performed during apoptosis. The H. pylori protein profile was analyzed by double-dimension electrophoresis (2-DE) and protein identification was performed by LC/NSI-MS/MS analysis. A significant increase in chromatin condensation and caspase-3 activity was seen in the AGS cells 12 h post-infection. The proteomic analysis demonstrated a significant increase in the expression of 19 proteins, from which five proteins were identified from H. pylori. Thirty-one spots were present during the pathogen-host interaction. In conclusion: H. pylori induced a significant increase in apoptosis in infected AGS cells 12 h post-infection, and the H. pylori proteins that were identified could be participating in the apoptotic event.

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Antimicrobial effects of antioxidants with and without clarithromycin on Helicobacter pylori

et al. 2005

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Increasing resistance to currently used antimicrobials has resulted in the evaluation of other agents that have antimicrobial activity against Helicobacter pylori. H. pylori American Type Culture Collection (ATCC) strain 49503 (a toxin-producing strain known to be associated with gastric cancer) was grown, a cell suspension prepared in 2 mL PBS and diluted 10-fold. One hundred microL of this cell suspension was added to vitamin C 0.5%, vitamin E 0.5%, garcinol 100 microg/mL, Protykin (containing 50% trans-resveratrol) 100 microg/mL and garcinol + Protykin 100 microg/mL in Lennox broth, and incubated for 16 h under microaerophilic conditions. Three replicates of 10 microL from each 10(-7) dilution tube were plated, colonies were counted after 16 h, and growth of H. pylori was confirmed by the CLO test. These colony counts were compared to control cultures without the addition of any antioxidants. The experiments were then repeated with the addition of 15 microg/mL of clarithromycin to experimental and control samples. Enhanced killing of H. pylori by 37.6% was noted when vitamin C was added, which increased to 66% when clarithromycin was added, compared to controls (p < 0.05). With garcinol and Protykin alone there was 91.4 and 87% killing of H. pylori, respectively, while a combination of garcinol + Protykin resulted in 90.8% killing compared to controls (p < 0.05). When clarithromycin was added, there was 76.3% increased killing with garcinol alone, 55.3% with Protykin alone, and 73.7% with garcinol + Protykin compared to controls (containing clarithromycin) (p < 0.05). Vitamin E had no effect on H. pylori growth compared to controls. We conclude from this study that some antioxidants such as vitamin C, garcinol and Protykin, but not vitamin E, may have potential as antimicrobial agents against H. pylori.

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Helicobacter pylori: recent advances in the study of its pathogenicity and prevention

Cited by 21 publications

References 133 publications

Low rate of recurrence of Helicobacter Pylori infection in spite of high clarithromycin resistance in Pakistan

Low rate of recurrence of Helicobacter Pylori infection in spite of high clarithromycin resistance in Pakistan

Comparative Proteomic Analysis of Helicobacter pylori-Expressed Proteins in Gastric Epithelial Cell Apoptosis (Supplementry Material)

Antimicrobial effects of antioxidants with and without clarithromycin on Helicobacter pylori

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