Hypoxia and Hypoxia‐Reoxygenation Potentiate <scp> <i>Helicobacter pylori</i> </scp> Infection and Gastric Epithelial Cell Proliferation

Hypoxia and HIF1 mediated upregulation of CEACAM6 in GECs. CEACAM6 significantly promoted ROS generation by inducing NOX4 in hypoxic GECs. HIF1α, CEACAM6, and NOX4 upregulation was detected in gastritis and GC tissues. H. pylori infection significantly increased in hypoxia-exposed GECs as compared to normoxic GECs. Infection of hypoxia-reoxygenated GECs also resulted in significantly increased CEACAM6 and NOX4-mediated ROS generation compared to normoxic GECs. In addition, adhesion of H. pylori, cytotoxin-associated gene A (CagA) translocation, and GEC proliferation were significantly enhanced in hypoxia-reoxygenated GECs. Collectively, this study established that hypoxia and hypoxia-reoxygenation of GECs facilitate H. pylori infection and infection-mediated GEC proliferation.

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Publication Details

Journal
Cancer Medicine
Published
2025-05-01
DOI
https://doi.org/10.1002/cam4.70860
Citations
3
Primary Topic
Helicobacter pylori-related gastroenterology studies
Type
article
Field-Weighted Citation Impact
6.02

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article

Hypoxia and Hypoxia‐Reoxygenation Potentiate Helicobacter pylori Infection and Gastric Epithelial Cell Proliferation

Pratyush Kumar Padhan, Asima Bhattacharyya, Shivaram Prasad Singh, Indrajit Poirah et al.
3 citations
Cancer Medicine
Helicobacter pylori-related gastroenterology studies
6.02
article

Hypoxia and Hypoxia‐Reoxygenation Potentiate Helicobacter pylori Infection and Gastric Epithelial Cell Proliferation

Pratyush Kumar Padhan, Asima Bhattacharyya, Shivaram Prasad Singh, Indrajit Poirah, Ashish Kumar Mishra, Pragyesh Dixit, Niranjan Rout, Debashish Chakraborty, Gaurav Nath, Hassan Ashktorab, Supriya Samal, S.P. Chakraborty, Duane T. Smoot
article en
3 citations

Abstract

Hypoxia and HIF1 mediated upregulation of CEACAM6 in GECs. CEACAM6 significantly promoted ROS generation by inducing NOX4 in hypoxic GECs. HIF1α, CEACAM6, and NOX4 upregulation was detected in gastritis and GC tissues. H. pylori infection significantly increased in hypoxia-exposed GECs as compared to normoxic GECs. Infection of hypoxia-reoxygenated GECs also resulted in significantly increased CEACAM6 and NOX4-mediated ROS generation compared to normoxic GECs. In addition, adhesion of H. pylori, cytotoxin-associated gene A (CagA) translocation, and GEC proliferation were significantly enhanced in hypoxia-reoxygenated GECs. Collectively, this study established that hypoxia and hypoxia-reoxygenation of GECs facilitate H. pylori infection and infection-mediated GEC proliferation.

Cancer MedicineVol. 14(9)
Meharry Medical College (US), Howard University (US), National Institute of Science Education and Research (IN), Homi Bhabha National Institute (IN), Institute of Physical Chemistry (PL), Polish Academy of Sciences (PL)
Department of Atomic Energy, Government of India
Openalex Percentile: Top 4%
Helicobacter pylori-related gastroenterology studies
6.02
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