Epigenetic Regulation of Tumor Suppressors by<i>Helicobacter pylori</i>Enhances EBV-Induced Proliferation of Gastric Epithelial Cells

Pandey, Saurabh; Jha, Hem Chandra; Shukla, Sanket K.; Shirley, Meghan K.; Robertson, Erle S.

doi:10.1128/mbio.00649-18

Cited by 35 publications

(60 citation statements)

References 64 publications

(88 reference statements)

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“…The supernatant from cell culture was collected and treated with DNAse. The viruses were concentrated by ultracentrifugation 23,500×g at 4°C for 1 h 30 min and quantified through qRT-PCR [27][28][29]. The infective dose of EBV was determined by infecting 25 × 10 4 AGS cells seeded in 6 well plates with 0, 25, 50, 75, 100, and 125 μl of the isolated virus.…”

Section: Animal Cell Cultures and H Pylori Culturesmentioning

confidence: 99%

“…To evaluate differential expressions of several kinases, both direct and indirect infection methods were used [27]. In the indirect approach, the effect of proteins secreted from bacteria was assessed; and in the direct approach the kinases that are mostly affected by adherence were evaluated.…”

Section: Assessment Of Kinase Expression Through a Secretory And Adhementioning

confidence: 99%

“…This model would give us access to investigate the effect of molecules secreted by H. pylori. Hence we used the 0.45 μm insert, which has been used for a similar purpose in the previous reports [27,43]. As the effect of adherence of H. pylori to gastric mucosa through CagA is linked to the severity of gastritis, it was intriguing to compare the effect of secretory proteins and adherence of bacteria in gastric cells infected with EBV [44][45][46].…”

Section: Assessment Of Kinase Expression Through a Secretory And Adhementioning

confidence: 99%

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Status of kinases in Epstein-Barr virus and Helicobacter pylori Coinfection in gastric Cancer cells

et al. 2020

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Background Helicobacter pylori (H. pylori) and Epstein - Barr virus (EBV) plays a significant role in aggressive gastric cancer (GC). The investigation of genes associated with these pathogens and host kinases may be essential to understand the early and dynamic progression of GC. Aim The study aimed to demonstrate the coinfection of EBV and H. pylori in the AGS cells through morphological changes, expression of the kinase and the probable apoptotic pathways. Methods Genomic DNA isolation of H. pylori and its characterization from clinical samples were performed. RT-qPCR of kinases was applied to scrutinize the gene expression of kinases in co-infected GC in a direct and indirect (separated through insert size 0.45 μm) H. pylori infection set up. Morphological changes in co-infected GC were quantified by measuring the tapering ends of gastric epithelial cells. Gene expression profiling of apoptotic genes was assessed through RT-qPCR. Results An interleukin-2-inducible T-cell kinase (ITK) showed significant upregulation with indirect H. pylori infection. Moreover, Ephrin type-B receptor six precursors (EPHB6) and Tyrosine-protein kinase Fyn (FYN) showed significant upregulation with direct coinfection. The tapering ends in AGS cells were found to be extended after 12 h. A total of 24 kinase genes were selected, out of which EPHB6, ITK, FYN, and TYK2 showed high expression as early as 12 h. These kinases may lead to rapid morphological changes in co-infected gastric cells. Likewise, apoptotic gene expression such as APAF-1 and Bcl2 family genes such as BAD, BID, BIK, BIM, BAX, AND BAK were significantly down-regulated in co-infected AGS cells. Conclusion All the experiments were performed with novel isolates of H. pylori isolated from central India, for the functional assessment of GC. The effect of coinfection with EBV was more profoundly observed on morphological changes in AGS cells at 12 h as quantified by measuring the tapering of ends. This study also identifies the kinase and apoptotic genes modulated in co-infected cells, through direct and indirect approaches. We report that ITK, EPHB6, TYK2, FYN kinase are enhanced, whereas apoptotic genes such as APAF-1, BIK, FASL, BAX are significantly down-regulated in AGS cells coinfected with EBV and H. pylori.

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Section: Animal Cell Cultures and H Pylori Culturesmentioning

confidence: 99%

Section: Assessment Of Kinase Expression Through a Secretory And Adhementioning

confidence: 99%

Section: Assessment Of Kinase Expression Through a Secretory And Adhementioning

confidence: 99%

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Status of kinases in Epstein-Barr virus and Helicobacter pylori Coinfection in gastric Cancer cells

et al. 2020

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“…It will be interesting to explore whether such mutually beneficial collaboration exists between H pylori and EBV in vivo. From a molecular perspective, previous studies showed that the virulence factor CagA from H pylori potentiated EBV‐mediated cell proliferation 72 . Similarly, EBV could inhibit protein tyrosine phosphatase SHP1, an antagonist of CagA, thereby enhancing the oncogenic action of CagA 73 .…”

Section: Future Directionsmentioning

confidence: 99%

Helicobacter pylori infection and eradication: Exploring their impacts on the gastrointestinal microbiota

2020

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The rapid development of microbiota research has remolded our view of human physiological and pathological processes. Among all the gastrointestinal microorganisms, Helicobacter pylori (H pylori) is probably the most notorious constituent. Although half of the adults worldwide are infected with H pylori, their clinical manifestations vary widely, suggesting other microorganisms beyond H pylori may play a role in determining clinical outcomes. Recently, many studies have put effort into elucidating the crosstalk within the human microbiota, some of which specifically explored the interplay between H pylori and other gastrointestinal microbial members. In this work, we reviewed these potential interactions. Meanwhile, the impacts of H pylori eradication therapy on gastrointestinal microbial homeostasis were summarized in terms of diversity, composition, functional capacity, and antibiotic resistance.

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“…The resulting SHP1 downregulation upregulates oncogenic H. pylori cytotoxin-associated gene A (CagA) phosphorylation [4]. Conversely, H. pylori CagA protein stimulates EBV-mediated epigenetic modifications and cell proliferation in a coinfection model [5]. Also, several cases show that the preceding infection of H. pylori promotes the development of EBVaGC [6].…”

Section: Introductionmentioning

confidence: 99%

Application of Biopsy Samples Used for Helicobacter pylori Urease Test to Predict Epstein–Barr Virus-Associated Cancer

et al. 2020

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Persistent gastric mucosal damage caused by Helicobacter pylori infection is a major risk factor for gastric cancer (GC). The Epstein–Barr virus (EBV) is also associated with GC. Most patients with EBV-associated GC are infected with H. pylori in East Asia. However, very few reports have described where and when both H. pylori and EBV infect the gastric mucosa. To clarify this, old biopsy samples used for the rapid urease test (RUT) were applied to count EBV genomic DNA (gDNA) copies using DNA probe quantitative polymerase chain reaction. DNA extracted from the gastric biopsy samples of 58 patients with atrophic gastritis was used to analyze the correlation between the degree of atrophic gastritis and the copy number of EBV gDNA. EBV was detected in 44 cases (75.9%), with viral copy numbers ranging from 12.6 to 4754.6. A significant correlation was found between patients with more than 900 copies of EBV gDNA and those with a more severe grade of atrophic gastritis (p = 0.041). This study shows that EBV can be detected in RUT samples in a manner that reduces patient burden.

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Epigenetic Regulation of Tumor Suppressors byHelicobacter pyloriEnhances EBV-Induced Proliferation of Gastric Epithelial Cells

Cited by 35 publications

References 64 publications

Status of kinases in Epstein-Barr virus and Helicobacter pylori Coinfection in gastric Cancer cells

Status of kinases in Epstein-Barr virus and Helicobacter pylori Coinfection in gastric Cancer cells

Helicobacter pylori infection and eradication: Exploring their impacts on the gastrointestinal microbiota

Application of Biopsy Samples Used for Helicobacter pylori Urease Test to Predict Epstein–Barr Virus-Associated Cancer

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