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, 21 (1), 96

Higher Glucose Level Can Enhance the H. Pylori Adhesion and Virulence Related With Type IV Secretion System in AGS Cells

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Higher Glucose Level Can Enhance the H. Pylori Adhesion and Virulence Related With Type IV Secretion System in AGS Cells

Shew-Meei Sheu et al. J Biomed Sci.

Abstract

Background: Hyperglycemia increases the risk of gastric cancer in H. pylori-infected patients. High glucose could increase endothelial permeability and cancer-associated signaling. These suggest high glucose may affect H. pylori or its infected status.We used two strains to investigate whether H. pylori growth, viability, adhesion and CagA-phosphorylation level in the infected-AGS cells were influenced by glucose concentration (100, 150, and 200 mg/dL).

Results: The growth curves of both strains in 200 mg/dL of glucose were maintained at the highest optimal density after 48 h and the best viability of both strains were retained in the same glucose condition at 72 h. Furthermore, adhesion enhancement of H. pylori was significantly higher in 200 mg/dL of glucose as compared to that in 100 and 150 mg/dL (p < 0.05). CagA protein also increased in higher glucose condition. The cell-associated CagA and phosphorylated-CagA was significantly increased in 150 and 200 mg/dL of glucose concentrations as compared to that of 100 mg/dL (p < 0.05), which were found to be dose-dependent.

Conclusion: Higher glucose could maintain H. pylori growth and viability after 48 h. H. pylori adhesion and CagA increased to further facilitate the enhancement of cell-associated CagA and phosphorylated CagA in higher glucose conditions.

Figures

Figure 1
Figure 1
H. pylori growth and viability was increased under higher glucose level after 48 hr. (A, B) Strain J99 and 43504 grew in Brucella broth containing 10% horse serum and different level of glucose (100, 150, 200 mg/dL). The optical density (OD) at 600 nm of bacterial growth was evaluated during 72 h. (C, D) Colony formation unit (CFU) of strain J99 and 43504 was determined at growth curve of 48 and 72 h. * indicated p < 0.05 (paired t test).
Figure 2
Figure 2
Adhesion ability of H. pylori increased under the treatment of higher glucose concentration. Strain J99 and 43504 growth in different level of glucose (100, 150, 200 mg/dL) was added to AGS cells with the pretreatment of the same glucose concentration (A, B) or the pretreatment of contrary concentration (200, 150, 100 mg/dL) (C, D). Relative adhesion ratio indicates that the adhesion of H. pylori in 100 mg/dL of glucose serve as the reference, and the bacterial adhesion value in 150 and 200 mg/dL of glucose was divided by the value of reference. *indicated a significant difference between the treatment of different glucose concentrations (paired t test, p < 0.05).
Figure 3
Figure 3
Figure 3 H. pylori CagA and phosphorylated CagA increased in higher glucose concentration. (A) BabA and CagA expression of H. pylori grown in three glucose concentrations. (B) The level of cell-associated CagA and phosphorylated CagA after H. pylori infecting AGS cells for 4 h. Thee glucose concentrations were 100, 150 and 200 mg/dL, respectively. *indicated a significant difference between the treatment of different glucose concentrations (paired t test, p < 0.05).

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References

    1. Price AB, Levi J, Dolby JM, Dunscombe PL, Smith A, Clark J, Stephenson ML. Campylobacter pyloridis in peptic ulcer disease: microbiology, pathology, and scanning electron microscopy. Gut. 1985;26:1183–1188. doi: 10.1136/gut.26.11.1183. - DOI - PMC - PubMed
    1. Rauws EA, Langenberg W, Houthoff HJ, Zanen HC, Tytgat GN. Campylobacter pyloridis-associated chronic active antral gastritis. A prospective study of its prevalence and the effects of antibacterial and antiulcer treatment. Gastroenterology. 1988;94:33–40. - PubMed
    1. Parsonnet J, Friedman GD, Vandersteen DP, Chang Y, Vogelman JH, Orentreich N, Sibley RK. Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med. 1991;325:1127–1131. doi: 10.1056/NEJM199110173251603. - DOI - PubMed
    1. Ataseven H, Demir M, Gen R. Effect of sequential treatment as a first-line therapy for Helicobacter pylori eradication in patients with diabetes mellitus. South Med J. 2010;103:988–992. doi: 10.1097/SMJ.0b013e3181eea6cc. - DOI - PubMed
    1. Zhou X, Zhang C, Wu J, Zhang G. Association between Helicobacter pylori infection and diabetes mellitus: a meta-analysis of observational studies. Diabetes Res Clin Pract. 2013;99:200–208. doi: 10.1016/j.diabres.2012.11.012. - DOI - PubMed

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