지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록· 키워드
오류제보하기
Helicobacter pylori is a potential cause for peptic ulcers which can make persistent chronic infection. Helicobacter pylori produce urease at low pH to neutralize the acidic environment to colonize the gastric mucosa. This investigation aimed to characterize H. pylori based on urease, adherence, motility, and biofilm activity and to determine the gene expression of SabA and BabA by real-time qRT-PCR. The reference culture H. pylori ATCC 49503 was employed in the current study. The characterization of H. pylori, such as biofilm, urease, adherence, and motility assays, was determined in acidic environments with the supplement of urea substrate. Real-time qRT-PCR was executed to find the possible explanation for the colonization by the genes actin, SabA, and BabA. The study indicated that urea substrate is important in biofilm activity, adherence, motility, and urease of H. pylori. Helicobacter pylori ATCC 49503 showed enhanced activity at pH 2.5 only when supplemented with urea substrate. Real-time qRT-PCR confirmed the positive and significant expression of the SabA and BabA genes in an acidic environment and its cooperative role in biofilm and the motility of H. pylori. The results propose that urease within H. pylori is necessary to neutralize the acidic niche and colonize effectively within the mucosal layers of the stomach. Additionally, the colonization and adaptability of H. pylori in the in vitro were dependant on urease and pH. Further studies are proposed to understand the colonization of clinical strains of H. pylori.
목차
Materials and Methods
Results
Discussion
Conclusion
References
참고문헌 (40)
참고문헌 신청
Abadi ATB. 2017. Strategies used by Helicobacter pylori to establish persistent infection. World J. Gastroenterol. 23, 2870–2882.
Ansari S and Yamaoka Y. 2017a. Helicobacter pylori BabA in adaptation for gastric colonization. World J. Gastroenterol. 23, 4158–4169.
Ansari S and Yamaoka Y. 2017b. Survival of Helicobacter pylori in gastric acidic territory. Helicobacter 22, e12386.
Ansari S and Yamaoka Y. 2019. Helicobacter pylori virulence factors exploiting gastric colonization and its pathogenicity. Toxins 11, 677.
Benktander J, Barone A, Johansson MM, and Teneberg S. 2018. Helicobacter pylori SabA binding gangliosides of human stomach. Virulence 9, 738–751.
Ansari S and Yamaoka Y. 2017a. Helicobacter pylori BabA in adaptation for gastric colonization. World J. Gastroenterol. 23, 4158–4169.
Ansari S and Yamaoka Y. 2017b. Survival of Helicobacter pylori in gastric acidic territory. Helicobacter 22, e12386.
Ansari S and Yamaoka Y. 2019. Helicobacter pylori virulence factors exploiting gastric colonization and its pathogenicity. Toxins 11, 677.
Benktander J, Barone A, Johansson MM, and Teneberg S. 2018. Helicobacter pylori SabA binding gangliosides of human stomach. Virulence 9, 738–751.
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