Gastric cancer risk evolves over time due to environmental, dietary, and lifestyle changes, including Helicobacter pylori (H. pylori)
infection and consumption of hot peppers (i.e.,
capsaicin). H. pylori
infection promotes gastric mucosal injury in the early phase of
capsaicin exposure. This relationship suggests a need to investigate the mechanism of how both H. pylori
infection and
capsaicin contribute to gastric
inflammation and lead to
gastric cancer. C57-Balb/c mice were infected with the H. pylori (SS1) strain and then fed
capsaicin (0.05% or 0.2 g/kg/day) or not. Consequently,
tumor size and phenotype were analyzed to determine the molecular mechanism driving the shift from
gastritis to
stomach cancer. Moreover, we used 2-difluoromethylornithine (DFMO) in mice to prevent gastric
tumorigenesis by reducing
inflammation and promoting recovery of disease-free stasis. This study provides evidence showing that a combination of H. pylori
infection and
capsaicin consumption leads to gastric
carcinogenesis mediated through
interleukin-6 (IL-6) stimulation with an incidence rate of 50%. The anti-inflammatory role of DFMO highlights the injurious effect of
inflammation in
gastric cancer development and the need to reduce gastric
inflammation for
cancer prevention by inhibiting
IL-6. Accordingly, preventive measures such as reduced
capsaicin consumption, H. pylori clearance, and DFMO treatment may lessen
gastric cancer incidence.