The Biology of<i>Helicobacter pylori</i>Infection, a Major Risk Factor for Gastric Adenocarcinoma

Pinto-Santini, Delia; Salama, Nina R.

doi:10.1158/1055-9965.epi-04-0784

Cited by 35 publications

(20 citation statements)

References 55 publications

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“…For the NSH57 strain background, the ID 50 was 30-fold higher than that of wild-type bacteria. As expected, the HP1081 null allele has a higher ID 50 than the wild type in the NSH79 background, in this case, 2,500-fold higher. By contrast, in the NSH57 background, the ID 50 was essentially indistinguishable from that of wild-type bacteria (1.5-fold higher).…”

Section: Vol 75 2007supporting

confidence: 83%

“…For the 50% infective dose (ID 50 ) experiments, the indicated strains were grown in liquid culture to mid-to late logarithmic phase and concentrated to give approximately 5 ϫ 10 8 bacteria per ml. Serial 10-fold dilutions were prepared and inoculated into each of five mice.…”

Section: Methodsmentioning

confidence: 99%

“…VacA, a secreted protein, has a vast array of activities linked to it, including membrane insertion, anion-conducting channel activity, alteration of transepithelial resistance, inhibition of antigen processing, and induction of apoptosis (50). Presumably, the loss of membrane integrity in the host cell increases nutrient availability at the host cell surface.…”

mentioning

confidence: 99%

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Identification of Helicobacter pylori Genes That Contribute to Stomach Colonization

et al. 2007

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Chronic infection of the human stomach by Helicobacter pylori leads to a variety of pathological sequelae, including peptic ulcer and gastric cancer, resulting in significant human morbidity and mortality. Several genes have been implicated in disease related to H. pylori infection, including the vacuolating cytotoxin and the cag pathogenicity island. Other factors important for the establishment and maintenance of infection include urease enzyme production, motility, iron uptake, and stress response. We utilized a C57BL/6 mouse infection model to query a collection of 2,400 transposon mutants in two different bacterial strain backgrounds for H. pylori genetic loci contributing to colonization of the stomach. Microarray-based tracking of transposon mutants allowed us to monitor the behavior of transposon insertions in 758 different gene loci. Of the loci measured, 223 (29%) had a predicted colonization defect. These included previously described H. pylori virulence genes, genes implicated in virulence in other pathogenic bacteria, and 81 hypothetical proteins. We have retested 10 previously uncharacterized candidate colonization gene loci by making independent null alleles and have confirmed their colonization phenotypes by using competition experiments and by determining the dose required for 50% infection. Of the genetic loci retested, 60% have strain-specific colonization defects, while 40% have phenotypes in both strain backgrounds for infection, highlighting the profound effect of H. pylori strain variation on the pathogenic potential of this organism.Helicobacter pylori, a bacterial pathogen of the human stomach, infects an estimated 50% of the population worldwide. Infection by H. pylori causes gastritis initially and, if allowed to persist, can induce a range of pathologies. It is the causative agent of most peptic ulcers, and other serious outcomes such as atrophic gastritis, intestinal metaplasia, and gastric cancer are correlated with long-term infections. It is not yet known whether these outcomes are due to specific factors produced by the organism or whether they result from chronic inflammation due to efficient and persistent colonization of the gastric mucosa. Thus, colonization and persistence factors may themselves constitute virulence factors for this organism.

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Section: Vol 75 2007supporting

confidence: 83%

Section: Methodsmentioning

confidence: 99%

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Identification of Helicobacter pylori Genes That Contribute to Stomach Colonization

et al. 2007

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“…Several epidemiological studies have detected an association between H. pylori infection and the risk of developing GC. The data are consistent among Caucasians, African-Americans and Asians (2)(3)(4). The northeast region of Thailand has the highest rate of H. pylori infection, although the north has the highest incidence and the south has the lowest incidence of GC (5).…”

Section: Introductionsupporting

confidence: 59%

Toll-Like Receptors are Associated with Helicobacter pylori Infection and Gastric Mucosa Pathology

Simawaranon

Wattanawongdon

Tongtawee

2017

Jundishapur J Microbiol

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Background: Toll-like receptors (TLRs) mediate recognition of Helicobacter pylori and initiate the innate immune response to infection. Toll-like receptors polymorphisms are thought to influence susceptibility to H. pylori infection and H. pylori-related diseases. Objectives: To investigate the association of TLR polymorphisms with the susceptibility to H. pylori infection and various types of gastritis in Thai patients. Methods: The single nucleotide polymorphisms (SNPs) TLR1 rs4833095, TLR2 rs3804099 and rs3804100, TLR4 rs10759932 and TLR10 rs10004195 were analysed in 400 gastritis patients by real-time PCR using a TaqMan SNP Genotyping Assay. The association between TLR polymorphisms and the risk of H. pylori infection was investigated in 196 uninfected and 204 H. pylori-infected patients. The associations between TLR genotypes and the risk of gastric pathology changes, including chronic gastritis (N = 312 cases) and precancerous gastric lesions/gastric cancer (GC) (N = 88 cases), were examined. Univariate analysis was used to determine odds ratios (ORs) with confidence intervals (95% CIs). Results: Patients with the CC -or TT homozygous genotype for TLR1 rs4833095 had a significantly increased risk of H. pylori susceptibility (OR = 2.28, 95% CI = 1.27 -7.60, P = 0.02 and OR = 1.34, 95% CI = 0.97 -1.86, P = 0.04, respectively). Patients with the AA homozygous genotype for TLR10 rs10004195 had a significantly increased risk of H. pylori susceptibility (OR = 1.28, 95% CI = 0.98 -1.76, P = 0.01) and exhibited a significantly increased risk of precancerous gastric lesions/GC (OR = 8.75, 95% CI = 2.78 -14.24, P < 0.01). Conclusions: Our findings suggest that the TLR1 rs4833095 and TLR10 rs10004195 polymorphisms are potential genetic risk factors that modify the H. pylori infection susceptibility and influence the clinical manifestation of chronic gastritis, precancerous gastric lesions and GC in Thai patients.

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“…Epidemiology investigation data showed that dietary factors, smoking and Helicobacter pylori infection played a role in high incidence and mortality rates of GC (Pinto-Santini and Salama, 2005). Importantly, molecular genetic studies have addressed the accumulations of multiple genes alterations involved in GC development, such as activation of oncogenes erbB-2, c-met, c-myc and k-ras, and inactivation of the tumor suppressor gene p53, Ecadherin, APC and RUNX3 (Li et al, 2002;Stock and Otto, 2005) in GC.…”

Section: Introductionmentioning

confidence: 99%

Identification and characterization of a novel p42.3 gene as tumor-specific and mitosis phase-dependent expression in gastric cancer

Fan

et al. 2007

Oncogene

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Multiple genetic alterations are attributed to gastric cancer (GC); however, only a few critical genes have been identified so far. In this study, we isolated and characterized a novel gene p42.3, represented as tumor-specific and mitosis phase-dependent expression protein in GC cell line BGC823. Our data showed that the expression of p42.3 was cell cycle-dependent in GC cell lines. Moreover, p42.3 was specifically expressed in primary GC tissues but not in the matched normal mucosa of stomach, and this gene was expressed in diverse embryonic tissues. Furthermore, significant suppression of cell proliferation and tumorigenicity were detected and G 2 /M phase arrest was observed in cell line BGC823 depleted of p42.3 expression by RNAi technique, and we confirmed the expression changes of cyclin B1 and Chk2 following the silence of p42.3. Taken together, we cloned and characterized p42.3 gene that was specifically expressed in GC tumors but not in normal gastric mucosa, and the gene was associated with M-phase regulation. Moreover, p42.3 might be involved in cell proliferation and tumorigenesis; therefore, this gene might have potential applications in the diagnosis or treatment of GC.

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The Biology ofHelicobacter pyloriInfection, a Major Risk Factor for Gastric Adenocarcinoma

Cited by 35 publications

References 55 publications

Identification of Helicobacter pylori Genes That Contribute to Stomach Colonization

Identification of Helicobacter pylori Genes That Contribute to Stomach Colonization

Toll-Like Receptors are Associated with Helicobacter pylori Infection and Gastric Mucosa Pathology

Identification and characterization of a novel p42.3 gene as tumor-specific and mitosis phase-dependent expression in gastric cancer

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