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Biochem Pharmacol. 2019 Feb 4. pii: S0006-2952(19)30033-4. doi: 10.1016/j.bcp.2019.02.003. [Epub ahead of print]

Helicobacter pylori infection promotes autophagy through Nrf2-mediated heme oxygenase upregulation in human gastric cancer cells.

Author information

1
Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea.
2
Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea; Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Sciences and Technology, Seoul National University, Seoul 08826, South Korea.
3
Department of Food Science and Technology, College of Knowledge-Based Services Engineering, Sungshin Women's University, Seoul 01133, South Korea.
4
Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul 08826, South Korea; Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Sciences and Technology, Seoul National University, Seoul 08826, South Korea; Cancer Research Institute, Seoul National University, Seoul 03080, South Korea. Electronic address: surh@plaza.snu.ac.kr.

Abstract

It has been reported that Helicobacter pylori (H. pylori) infection is one of the primary causes of gastritis and peptic ulcer diseases. More than 50% of the world's population is supposed to be infected by this bacterium. However, 90% of infected patients are asymptomatic, suggesting the existence of host defense mechanisms. Nrf2 is a transcription factors that plays a key role in cellular defence against oxidative stress and inflammation. Autophagy, an autodigestive process that degrades cellular organelles and proteins, plays an important role in maintaining cellular homeostasis. To investigate the molecular mechanisms responsible for cellular adaptive response to H. pylori induced gastric inflammation, human gastric epithelial cells and mice were infected with H. pylori. H. pylori infection induced expression of microtubule-associated light chain3 (LC3), an autophagic marker, through accumulation of reactive oxygen species and subsequently Nrf2 nuclear translocation in AGS cells. Furthermore, Nrf2-induced LC3 up-regulation was mediated by heme oxygenase-1 and its by-product, carbon monoxide. Taken together, Nrf2 may be considered to play a role in cellular adaptive response to H. pylori-induced gastritis by inducing autophagy.

KEYWORDS:

Autophagy; Carbon monoxide; Helicobacter pylori; Heme oxygenase; Nrf2

PMID:
30731075
DOI:
10.1016/j.bcp.2019.02.003

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