Helicobacter pylori-induced NF-κB: trailblazer for gastric pathophysiology

Area of Science:

• Immunology
• Microbiology
• Gastroenterology

Background:

• Nuclear factor-kappa B (NF-κB) signaling pathways regulate immune and stress responses.
• Helicobacter pylori utilizes ADP-L-glycero-β-D-manno-heptose (ADP-heptose) to activate NF-κB pathways.
• H. pylori-induced NF-κB activation contributes to gastric pathophysiology and disease.

Purpose of the Study:

• To review H. pylori- and NF-κB-dependent cellular alterations in gastric pathophysiology.
• To discuss implications for diagnosing and treating gastric diseases, including gastric cancer (GC).
• To highlight the role of gastric organoids in personalized medicine for chemotherapy.

Main Methods:

• Review of scientific literature on NF-κB signaling, H. pylori, and gastric diseases.
• Analysis of H. pylori-mediated NF-κB pathway activation mechanisms.
• Exploration of therapeutic strategies including small molecule inhibitors and epigenetic therapy.

Main Results:

• H. pylori infection leads to maladaptive cellular responses via NF-κB.
• These alterations contribute to the development of gastric diseases.
• Gastric organoid biobanks offer a platform for predicting patient response to chemotherapy.

Conclusions:

• NF-κB pathway dysregulation by H. pylori is central to gastric pathophysiology.
• Targeting NF-κB and utilizing epigenetic therapies show promise for gastric cancer treatment.
• Patient-derived gastric organoids are crucial for advancing personalized medicine in oncology.