Abstract
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.
Highlights
The Centers for Disease Control and Prevention estimates that roughly two-thirds of the population of the world harbor Helicobacter pylori (H. pylori), a bacterium that colonizes the stomach and duodenum [1,2]
To investigate the role of capsaicin consumption in the progression of H. pylori-associated gastric cancer, we developed a mouse model treated with a combination of capsaicin and H. pylori infection-induced gastritis, leading to gastric cancer
Macroscopic morphometric analysis revealed that capsaicin consumption induced gastric inflammation as the initiating process, which led to tumor development in the stomachs of mice with H. pylori infection (Figure 1b)
Summary
The Centers for Disease Control and Prevention estimates that roughly two-thirds of the population of the world harbor Helicobacter pylori (H. pylori), a bacterium that colonizes the stomach and duodenum [1,2]. H. pylori infection is a known risk factor for gastrointestinal illnesses like chronic gastritis, peptic ulcers, and stomach cancer [3,4,5]. In 2001, an epidemiologic study demonstrated that patients infected with H. pylori were nearly six times more likely to develop gastric cancer compared to uninfected people. Other gastric cancer risk factors include host [6,7], dietary, and lifestyle practices including capsaicin consumption, stress levels, and ingestion of inflammatory foods or beverages. The etiology of gastric cancer is influenced by bacterial variability, along with host genetic and environmental factors; the molecular mechanisms governing these factors have not been fully elucidated [8,9,10,11].
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