Review
Oncology
Michelle C. C. Lim, Phatcharida Jantaree, Michael Naumann
Summary: Helicobacter pylori is a pathogenic bacterium that resides in the stomach lining and causes inflammation called type B gastritis. The chronic inflammation induced by H. pylori and other factors may lead to the development of stomach neoplasms and adenocarcinoma. Dysregulation of cellular processes in the stomach lining and microenvironment is a characteristic of H. pylori infection. In this review, we discuss the contradictory role of H. pylori in promoting or suppressing apoptosis in gastric epithelial cells and highlight the key processes in the microenvironment that contribute to apoptosis and gastric carcinogenesis.
Article
Medicine, Research & Experimental
Jennifer M. Noto, M. Blanca Piazuelo, Shailja C. Shah, Judith Romero-Gallo, Jessica L. Hart, Chao Di, James D. Carmichael, Alberto G. Delgado, Alese E. Halvorson, Robert A. Greevy, Lydia E. Wroblewski, Ayushi Sharma, Annabelle B. Newton, Margaret M. Allaman, Keith T. Wilson, M. Kay Washington, M. Wade Calcutt, Kevin L. Schey, Bethany P. Cummings, Charles R. Flynn, Joseph P. Zackular, Richard M. Peek
Summary: This study reveals that Helicobacter pylori enhances gastric injury under conditions of iron deficiency and that this phenomenon is closely associated with altered bile acid metabolism. Deoxycholic acid (DCA) is identified as a carcinogenic bile acid that can further exacerbate gastric injury and promote the translocation of the H. pylori oncoprotein CagA into host cells. Conversely, the use of bile acid sequestrants can attenuate H. pylori-induced injury. Furthermore, cumulative use of bile acid sequestrants is significantly associated with a reduced risk of gastric cancer in human populations. These findings demonstrate the importance of bile acid metabolism in H. pylori-induced gastric injury and carcinogenesis.
JOURNAL OF CLINICAL INVESTIGATION
(2022)
Article
Biochemistry & Molecular Biology
Olga Sokolova, Michael Naumann
Summary: Gastric cancer is a major cause of cancer-related deaths globally, and its development is influenced by genetic predisposition, environmental factors, and Helicobacter pylori infection. Matrix metalloproteinases (MMPs) play an active role in the progression of gastric cancer, with bacterial dependence being less significant in later stages.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Immunology
Quynh Anh Nguyen, Leonard Schmitt, Raquel Mejias-Luque, Markus Gerhard
Summary: Helicobacter pylori uses its virulence factors, including the adhesin HopQ, to initiate and regulate the host's inflammatory responses during chronic infection in the human stomach. The interaction between HopQ and human CEACAMs allows the translocation of the CagA protein into host cells through the T4SS. The HopQ-CEACAM interaction plays a crucial role in the adhesion of H. pylori to host cells and modulation of cellular processes.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Biotechnology & Applied Microbiology
Jinglei Liu, Fangxu Zhang, Zheming Zhang, Chunning Zheng
Summary: This study found that Everolimus has a pharmacological role in protecting gastric epithelial cells from H.pylori-induced damage. It achieves this by reducing oxidative stress and inhibiting inflammatory response, as well as inhibiting the attachment of monocytes to epithelial cells.
Article
Biochemistry & Molecular Biology
Jonas Wizenty, Stefanie Muellerke, Marina Kolesnichenko, Julian Heuberger, Manqiang Lin, Anne-Sophie Fischer, Hans-Joachim Mollenkopf, Hilmar Berger, Frank Tacke, Michael Sigal
Summary: Helicobacter pylori is a pathogen that causes chronic gastritis by colonizing the stomach. This study found that Rspo3 signaling through Lgr4 regulates the proliferation of stem cells and induces NF-kappa B activity in proliferating stem cells. The invasion of H. pylori leads to Lgr4-driven NF-kappa B activation, resulting in expansion of the gland base module and chemokine expression in stem cells, leading to gland hyperplasia and neutrophil recruitment.
Article
Medicine, General & Internal
Yoshiaki Usui, Yukari Taniyama, Mikiko Endo, Yuriko N. Koyanagi, Yumiko Kasugai, Isao Oze, Hidemi Ito, Issei Imoto, Tsutomu Tanaka, Masahiro Tajika, Yasumasa Niwa, Yusuke Iwasaki, Tomomi Aoi, Nozomi Hakozaki, Sadaaki Takata, Kunihiko Suzuki, Chikashi Terao, Masanori Hatakeyama, Makoto Hirata, Kokichi Sugano, Teruhiko Yoshida, Yoichiro Kamatani, Hidewaki Nakagawa, Koichi Matsuda, Yoshinori Murakami, Amanda B. Spurdle, Keitaro Matsuo, Yukihide Momozawa
Summary: This study reveals that certain genetic variants associated with Helicobacter pylori infection can increase the risk of gastric cancer. Individuals carrying these genetic variants and infected with H. pylori have an even higher risk of developing gastric cancer.
NEW ENGLAND JOURNAL OF MEDICINE
(2023)
Review
Biochemistry & Molecular Biology
Silvia Salvatori, Irene Marafini, Federica Laudisi, Giovanni Monteleone, Carmine Stolfi
Summary: H. pylori infection contributes to the onset and development of gastric cancer through the mechanisms of chronic inflammation and DNA damage to gastric epithelial cells.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Nutrition & Dietetics
Moon-Young Song, Da-Young Lee, Young-Min Han, Eun-Hee Kim
Summary: Research has shown that Korean propolis (KP) has anti-inflammatory effects on gastric mucosal injury caused by Helicobacter pylori infection. KP inhibits the growth of H. pylori and reduces the expression of virulence factors. It also decreases inflammation and pathological damage by suppressing the NF-kappa B signaling pathway. These findings suggest that KP could be a natural supplement for patients with gastric mucosal injury caused by H. pylori infection.
Article
Oncology
Jee Hyun Kang, Suyoung Park, Jinhyung Rho, Eun-Ju Hong, Young-Eun Cho, Young-Suk Won, Hyo-Jung Kwon
Summary: IL-17A promotes gastric carcinogenesis, potentially through the regulation of the IL-17RC/NF-κB/NOX1 pathway. This finding provides a new target for the treatment of gastric cancer.
Article
Multidisciplinary Sciences
Carmen Aguilar, Mindaugas Pauzuolis, Malvika Pompaiah, Ehsan Vafadarnejad, Panagiota Arampatzi, Mara Fischer, Dominik Narres, Mastura Neyazi, Ozge Kayisoglu, Thomas Sell, Nils Bluethgen, Markus Morkel, Armin Wiegering, Christoph-Thomas Germer, Stefan Kircher, Andreas Rosenwald, Antoine-Emmanuel Saliba, Sina Bartfeld
Summary: In this study, it was found that Helicobacter pylori prefers to attach to differentiated cells in the pit region of gastric units. Organoid models were used to validate this phenomenon, and it was discovered that differentiated pit cells with high levels of GKN1, GKN2 and PSCA were more susceptible to H. pylori attachment and CagA translocation. It was also found that attachment was unrelated to the expression of MUC5AC or PSCA, but relied on bacterial chemotaxis towards host cell-released urea, which was proportional to the size of the host cell.
NATURE COMMUNICATIONS
(2022)
Article
Oncology
Barbara Kiesewetter, Christiane Copie-Bergman, Michael Levy, Fangtian Wu, Jehan Dupuis, Caroline Barau, Luca Arcaini, Marco Paulli, Marco Lucioni, Arturo Bonometti, Antonio Salar, Concepcion Fernandez-Rodriguez, Miguel A. Piris, Francesco Cucco, Rachel Dobson, Yan Li, Zi Chen, Cyrielle Robe, Ingrid Simonitsch-Klupp, Andrew Wotherspoon, Markus Raderer, Ming Qing Du
Summary: The study reveals that H. pylori negative gastric MALT lymphoma is characterized by frequent genetic changes in the NF-kappa B signaling pathways. However, these genetic changes do not show significant correlation with clinicopathological parameters, and patients treated with systemic therapy have significantly better progression-free survival compared to those treated with antibiotics.
Article
Microbiology
Shweta Mahant, Amlan Chakraborty, Anup Som, Shubham Mehra, Kunal Das, Asish Kumar Mukhopadhyay, Valentina Gehlot, Sudeep Bose, Rajashree Das
Summary: The study proposes a new model for cell fate decision upon Helicobacter pylori infection, with key factors including Tipα, Nucleolin, and Ras. Simulation data and clinical research indicate that binding of Tipα to Nucleolin promotes inflammation, while binding to Nucleolin leads to cell proliferation.
CURRENT MICROBIOLOGY
(2021)
Article
Oncology
Qun Zhang, Ying Ni, Xiaofei Zhi, Jiwei Wang, Zheng Li, Jie Tang, Linjun Wang, Weizhi Wang, Zekuan Xu
Summary: In patients with gastric cancer infected with H. pylori, the expression of APRIL was upregulated and promoted the proliferation, migration, invasion, viability, and metastasis of GC cells through miR-145. Furthermore, APRIL induced gastric tumorigenicity by activating the NF-kappa B pathway. These findings lay the groundwork for a more in-depth analysis of APRIL in gastric cancer risk and prognosis.
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
(2021)
Review
Biochemistry & Molecular Biology
Gunter Maubach, Michael Vieth, Francesco Boccellato, Michael Naumann
Summary: NF-03 signaling pathways are crucial for immune response and gastric pathophysiology, and their alterations induced by Helicobacter pylori infection have implications for gastric diseases.
TRENDS IN MOLECULAR MEDICINE
(2022)