Persistence of Helicobacter pylori Infection: Genetic and Epigenetic Diversity

Benghezal, Mohammed; Gauntlett, Jonathan C.; Debowski, Aleksandra W.; Fulurija, Alma; Nilsson, Hans‐Olof; JamesMarshall, Barry

doi:10.5772/57428

Cited by 6 publications

(6 citation statements)

References 317 publications

(483 reference statements)

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“…Because strain-specific genes could be involved in gastric adaptation during coevolution, this flexible gene pool was extensively investigated in many strains worldwide. In silico analysis of the two H. pylori genomes revealed that both housekeeping genes and virulence genes are transferred between H. pylori strains [278,279]. Using conditional mutants to study the role of genes in persistence.…”

Section: Comparative Genomicsmentioning

confidence: 99%

Trends in Helicobacter pylori Infection

Röesler¹

2014

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is a pharmacist biochemist and holds a Master's Degree in Pharmacology and a Doctoral Degree in Basic Sciences -Internal Medicine from State University of Campinas (Campinas, SP, Brazil), where she has identified the principal genotypes of Helicobacter pylori in patients with chronic gastritis, peptic ulcer disease and early and advanced gastric adenocarcinoma through molecular biology techniques. She has published her work in several peer-reviewed journals and given oral and poster presentations at various congresses. She is a member of the Helicobacter pylori Research Group Study from State University of Campinas, including the study of etiology, epidemiology and physiopathology of gastrointestinal diseases. She has also participated in research that reports the possible relationship between H. pylori infection and idiopathic thrombocytopenic purpura, as well as between H. pylori infection and liver diseases. Her postdoctoral work includes the study of H. pylori in extradigestive manifestations, especially regarding pancreas and perigastric lymphonodes from patients with gastric adenocarcinoma. ContentsPreface XIII Section 1 Immunopathology and Genetic Diversity 1

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Section: Comparative Genomicsmentioning

confidence: 99%

Trends in Helicobacter pylori Infection

Röesler¹

2014

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“…However, rather than participating in mismatch repairing, it suppresses homeologous recombination mediated by RecA 6 , 7 . Compared to E. coli , H. pylori is also missing a number of elements responsible for direct repair of DNA damage such as Ada methyltransferase, AlkB oxidative demethylase and Phr/Spl photolyase, as well as several gylcosylases and endonucleases involved in base excision repair including MutM, Tag, AlkA, Mpg, YgjF, Nei and Nfo 8 . On the other hand, the presence of a DNA polymerase I that lacks proof-reading activity also contributes to the generation of genomic plasticity in H. pylori 9 …”

Section: Introductionmentioning

confidence: 99%

Quantum changes inHelicobacter pylorigene expression accompany host-adaptation

Chua

Wise

Khosravi

et al. 2016

DNA Res

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Helicobacter pylori is a highly successful gastric pathogen. High genomic plasticity allows its adaptation to changing host environments. Complete genomes of H. pylori clinical isolate UM032 and its mice-adapted serial derivatives 298 and 299, generated using both PacBio RS and Illumina MiSeq sequencing technologies, were compared to identify novel elements responsible for host-adaptation. The acquisition of a jhp0562-like allele, which encodes for a galactosyltransferase, was identified in the mice-adapted strains. Our analysis implies a new β-1,4-galactosyltransferase role for this enzyme, essential for Ley antigen expression. Intragenomic recombination between babA and babB genes was also observed. Further, we expanded on the list of candidate genes whose expression patterns have been mediated by upstream homopolymer-length alterations to facilitate host adaption. Importantly, greater than four-fold reduction of mRNA levels was demonstrated in five genes. Among the down-regulated genes, three encode for outer membrane proteins, including BabA, BabB and HopD. As expected, a substantial reduction in BabA protein abundance was detected in mice-adapted strains 298 and 299 via Western analysis. Our results suggest that the expression of Ley antigen and reduced outer membrane protein expressions may facilitate H. pylori colonisation of mouse gastric epithelium.

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“…We have previously reviewed the occurrence of phase variable genes and their role in generating phenotypic diversity in H. pylori [ 11 ]. Studies have identified potential phase-variable genes in H. pylori , including members of RM systems, and experimental evidence exists to demonstrate the presence of functional phasevarions [ 6 ],[ 12 ],[ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Phase-variable restriction/modification systems are required for Helicobacter pylori colonization

et al. 2014

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BackgroundOne mechanism utilized by bacterial pathogens for host adaptation and immune evasion is the generation of phenotypic diversity by the phasevarion that results from the differential expression of a suite of genes regulated by the activity of a phase-variable methyltransferase within a restriction modification (RM) system. Phasevarions are active in Helicobacter pylori, however there have been no studies investigating the significance of phase-variable RM systems on host colonization.MethodsTwo mutant types incapable of phase variation were constructed; a clean deletion mutant (‘DEL’) and a mutant (‘ON’) where the homopolymeric repeat was replaced with a non-repeat synonymous sequence, resulting in expression of the full-length protein. The resulting mutants were assessed for their colonisation ability in the mouse model.ResultsFive phase-variable genes encoding either methyltransferases or members of RM systems were found in H. pylori OND79. Our mutants fell into three categories; 1, those with little effect on colonization, 2, those where expression of the full-length protein was detrimental, 3, those where both mutations were detrimental.ConclusionsOur results demonstrated that phase-variable methyltransferases are critical to H. pylori colonization, suggesting that genome methylation and generation of epigenetic diversity is important for colonization and pathogenesis. The third category of mutants suggests that differential genome methylation status of H. pylori cell populations, achieved by the phasevarion, is essential for host adaptation. Studies of phase-variable RM mutants falling in the two other categories, not strictly required for colonization, represent a future perspective to investigate the role of phasevarion in persistence of H. pylori.

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Persistence of Helicobacter pylori Infection: Genetic and Epigenetic Diversity

Cited by 6 publications

References 317 publications

Trends in Helicobacter pylori Infection

Trends in Helicobacter pylori Infection

Quantum changes inHelicobacter pylorigene expression accompany host-adaptation

Phase-variable restriction/modification systems are required for Helicobacter pylori colonization

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