Characterization of East-Asian Helicobacter pylori encoding Western EPIYA-ABC CagA

Tissera, Kavinda; Kim, Myeong-A; Lai, Jing; Angulmaduwa, Sacheera; Kim, Aeryun; Merrell, D. Scott; Kim, Jihye; Su, Haibo; Heon, Jeong

doi:10.1007/s12275-022-1483-7

Cited by 2 publications

(1 citation statement)

References 60 publications

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“…Helicobacter pylori have a high intraspecific genetic diversity, and most studies have focused on the identification of strain specificity related to gastric cancer (Tissera et al, 2022). The pathogenic mechanism of H. pylori may be related to many pathogenic factors of the bacteria, such as genes encoding outer membrane proteins (babA, oipA, sabA, and hopQ), exercise genes (flaA and flaB), and iceA, of which the CagA, VacA, activating protein A of peptic ulcer, and adhesins are particularly important (Da Costa et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Characteristics of different types of Helicobacter pylori: New evidence from non-amplified white light endoscopy

Liu

Kong²,

Hui³

et al. 2023

Front. Microbiol.

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BackgroundDifferent types of Helicobacter pylori (H. pylori) were analyzed to determine their infection characteristics using serology, pathology, and non-magnification white light endoscopy combined with the Kimura–Takemoto classification, and the regular arrangement of collecting venules (RAC) as well.Materials and methodsA retrospective analysis of 685 inpatients who have completed the 14C-urea breath test, the H. pylori antibody typing classification, the serum gastric function tests (PGI/PGII/G-17), the endoscope detection, and the pathological examinations.ResultsThe levels of PGI, PGII, and G-17 were in descending order from the type I H. pylori infection group to the type II H. pylori infection group than the control group (F = 14.31; 26.23; 9.12, P < 0.01). Using the Kimura–Takemoto classification, there were significant differences among the three groups of different degrees of atrophy (χ2=29.81; 482.78; 292.5, P< 0.01). Based on the characteristics of RAC, the H. pylori infection rates were in descending order from the type I H. pylori infection group to the type II H. pylori infection group than the control group (χ2= 200.39; 174.72; 143.51, P < 0.01). The type I H. pylori infection group had higher grades than those of the type II H. pylori infection group in the OLGA and OLGIM staging systems, while the differences are statistically significant only in the OLGA staging system (χ2=10.63, P < 0.05).ConclusionWith the aid of non-amplified white light endoscopy, we found new evidence of type I H. pylori infection accelerating the progression of gastric mucosal atrophy through the degree of atrophy and the range of infection, whereas type II H. pylori infection has a low ability of migration and atrophy progression. Individual virulence factor-based eradication therapy may be a better choice in future.

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Section: Discussionmentioning

confidence: 99%

Characteristics of different types of Helicobacter pylori: New evidence from non-amplified white light endoscopy

Liu

Kong²,

Hui³

et al. 2023

Front. Microbiol.

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Amino acid deletions at positions 893 and 894 of cytotoxin-associated gene A protein affect Helicobacter pylori gastric epithelial cell interactions

Xue,

Gong,

et al. 2024

World J Gastroenterol

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BACKGROUND Helicobacter pylori (H. pylori ) persistently colonizes the human gastric mucosa in more than 50% of the global population, leading to various gastroduodenal diseases ranging from chronic gastritis to gastric carcinoma. Cytotoxin-associated gene A (CagA) protein, an important oncoprotein, has highly polymorphic Glu-Pro-Ile-Tyr-Ala segments at the carboxyl terminus, which play crucial roles in pathogenesis. Our previous study revealed a significant association between amino acid deletions at positions 893 and 894 and gastric cancer. AIM To investigate the impact of amino acid deletions at positions 893 and 894 on CagA function. METHODS We selected a representative HZT strain from a gastric cancer patient with amino acid deletions at positions 893 and 894. The cagA gene was amplified and mutated into cagA -NT and cagA -NE (sequence characteristics of strains from nongastric cancer patients), cloned and inserted into pAdtrack-CMV, and then transfected into AGS cells. The expression of cagA and its mutants was examined using real-time polymerase chain reaction and Western blotting, cell elongation via cell counting, F-actin cytoskeleton visualization using fluorescence staining, and interleukin-8 (IL-8) secretion via enzyme-linked immunosorbent assay. RESULTS The results revealed that pAdtrack/cagA induced a more pronounced hummingbird phenotype than pAdtrack/cagA -NT and pAdtrack/cagA -NE (40.88 ± 3.10 vs 32.50 ± 3.17, P < 0.001 and 40.88 ± 3.10 vs 32.17 ± 3.00, P < 0.001) at 12 hours after transfection. At 24 hours, pAdtrack/cagA- NE induced significantly fewer hummingbird phenotypes than pAdtrack/cagA and pAdtrack/cagA- NT (46.02 ± 2.12 vs 53.90 ± 2.10, P < 0.001 and 46.02 ± 2.12 vs 51.15 ± 3.74, P < 0.001). The total amount of F-actin caused by pAdtrack/cagA was significantly lower than that caused by pAdtrack/cagA- NT and pAdtrack/cagA- NE (27.54 ± 17.37 vs 41.51 ± 11.90, P < 0.001 and 27.54 ± 17.37 vs 41.39 ± 14.22, P < 0.001) at 12 hours after transfection. Additionally, pAdtrack/cagA induced higher IL-8 secretion than pAdtrack/cagA- NT and pAdtrack/cagA- NE at different times after transfection. CONCLUSION Amino acid deletions at positions 893 and 894 enhance CagA pathogenicity, which is crucial for revealing the pathogenic mechanism of CagA and identifying biomarkers of highly pathogenic H. pylori .

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Characterization of East-Asian Helicobacter pylori encoding Western EPIYA-ABC CagA

Cited by 2 publications

References 60 publications

Characteristics of different types of Helicobacter pylori: New evidence from non-amplified white light endoscopy

Characteristics of different types of Helicobacter pylori: New evidence from non-amplified white light endoscopy

Amino acid deletions at positions 893 and 894 of cytotoxin-associated gene A protein affect Helicobacter pylori gastric epithelial cell interactions

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