Correlation between<i>Helicobacter pylori</i>OipA Protein Expression and<i>oipA</i>Gene Switch Status

Kudo, Takahiko; Nurgalieva, Zhannat Z.; Conner, Margaret E.; Crawford, Sue E.; Odenbreit, Stefan; Haas, Rainer; Graham, David Y.; Yamaoka, Yoshio

doi:10.1128/jcm.42.5.2279-2281.2004

Cited by 47 publications

(37 citation statements)

References 13 publications

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“…Fifty microliters were plated onto Skirrow's plates with 5% sheep blood and incubated for 96 h under microaerobic conditions as described (4). OipA expression was determined by Western blot on bacterial lysates as previously described (18).…”

Section: Methodsmentioning

confidence: 99%

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Regulation of Gastric Carcinogenesis by Helicobacter pylori Virulence Factors

et al. 2008

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Helicobacter pylori is the strongest known risk factor for gastric adenocarcinoma, and strains that possess the cag secretion system, which translocates the bacterial effector CagA into host cells, augment cancer risk. H. pylori strains that express the vacuolating cytotoxin or the outer membrane protein OipA are similarly associated with severe pathologic outcomes. We previously reported that an in vivo adapted H. pylori strain, 7.13, induces gastric adenocarcinoma in rodent models of gastritis. In the current study, we used carcinogenic strain 7.13 as a prototype to define the role of virulence constituents in H. pylori-mediated carcinogenesis. Mongolian gerbils were infected with wild-type strain 7.13 or cagA À , vacA À , or oipA À mutants for 12 to 52 weeks. All infected gerbils developed gastritis; however, inflammation was significantly attenuated in animals infected with the cagA À but not the vacA À or oipA À strains. Gastric dysplasia and cancer developed in >50% of gerbils infected with either the wild-type or vacA À strain but in none of the animals infected with the cagA À strain. Inactivation of oipA decreased B-catenin nuclear localization in vitro and reduced the incidence of cancer in gerbils. OipA expression was detected significantly more frequently among H. pylori strains isolated from human subjects with gastric cancer precursor lesions versus persons with gastritis alone. These results indicate that loss of CagA prevents the development of cancer in this model. Inactivation of oipA attenuates B-catenin nuclear translocation and also decreases the incidence of carcinoma. In addition to defining factors that mediate H. pylori-induced cancer, these results provide insight into mechanisms that may regulate the development of other malignancies arising within the context of inflammatory states. [Cancer Res 2008;68(2):379-87]

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Section: Methodsmentioning

confidence: 99%

“…Expression of OipA is regulated by slipped strand mispairing within a CT rich dinucleotide repeat region located in the 5 ¶ region of the gene (13,16). Recent reports have shown that OipA coregulates proinflammatory cytokine expression and mediates adherence of H. pylori to gastric epithelial cells (13)(14)(15)(16)(17)(18)(19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Gastric Carcinogenesis by Helicobacter pylori Virulence Factors

et al. 2008

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“…Immunoblotting-Anti-AlpA (AK214) (8), anti-AlpB (AK262) (9), anti-BabA (AK277) (18), and anti-OipA antisera (AK282) (19) were used as primary antibodies at a 1:5,000 dilution. Anti-CagA and anti-VacA antibodies (Austral Biologicals, San Ramon, CA) were used at a 1:3,000 dilution.…”

Section: Methodsmentioning

confidence: 99%

Functional and Intracellular Signaling Differences Associated with the Helicobacter pylori AlpAB Adhesin from Western and East Asian Strains

Lü

Beswick³

et al. 2007

Journal of Biological Chemistry

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“…The cag PAI is a 40-kb genome segment that encodes for f30 genes (1). OipA is an outer membrane protein of which the expression is transcriptionally regulated by a slipped-strand mispairing of the CT dinucleotide repeats in the 5 ¶ region of the gene (2,3). The majority of cag PAI-positive bacterial isolates are also OipA positive (4).…”

Section: Introductionmentioning

confidence: 99%

Balance between Polyoma Enhancing Activator 3 and Activator Protein 1 Regulates Helicobacter pylori–Stimulated Matrix Metalloproteinase 1 Expression

Lü

Sun

et al. 2006

Cancer Research

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Helicobacter pylori infection and elevated expression of tissue matrix metalloproteinase 1 (MMP-1) are both associated with gastric cancer. We investigated the regulation of MMP-1 expression during H. pylori infection. Real-time reverse transcription-PCR was used to examine mucosal MMP-1 mRNA levels in 55 patients with gastric cancers and 61 control patients. Increased MMP-1 mRNA levels in the gastric mucosa and epithelial cells were observed in H. pylori infections in which both the cag pathogenicity island (PAI) and outer inflammatory protein A (OipA) were expressed. The combined induction of c-fos, c-jun, and polyoma enhancing activator-3 (pea-3) by H. pylori caused maximal increase in MMP-1 expression. Activation of the MMP-1 promoter by H. pylori involved occupation of the activator protein 1 (AP-1) sites at À72 and À181 and, surprisingly, vacancy of the À88 PEA-3 site. Electrophoretic mobility shift, supershift, and chromatin immunoprecipitation assays showed increased binding of c-Fos and c-Jun to the À72 and À181 AP-1 sites during H. pylori infection. Importantly, during wild-type H. pylori infection, we detected increased PEA-3 binding to the À72AP-1 site and decreased PEA-3 binding to the À88 PEA-3 site. However, during infection with the cag PAI and oipA mutants, PEA-3 binding to the À88 site was detected. MMP-1 and pea-3 activities are increased in gastric cancers. Maximal activation of MMP-1 transcription requires the cag PAI and OipA, which regulate AP-1 and PEA-3 binding. Thus, cag PAI and OipA provide a possible link between bacterial virulence factors and important host factors related to disease pathogenesis.

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Correlation betweenHelicobacter pyloriOipA Protein Expression andoipAGene Switch Status

Cited by 47 publications

References 13 publications

Regulation of Gastric Carcinogenesis by Helicobacter pylori Virulence Factors

Regulation of Gastric Carcinogenesis by Helicobacter pylori Virulence Factors

Functional and Intracellular Signaling Differences Associated with the Helicobacter pylori AlpAB Adhesin from Western and East Asian Strains

Balance between Polyoma Enhancing Activator 3 and Activator Protein 1 Regulates Helicobacter pylori–Stimulated Matrix Metalloproteinase 1 Expression

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