- The H/K-ATPase-IL-1β transgenic mouse model is engineered to specifically express human interleukin-1β (IL-1β) in the stomach mucosa under the control of the H/K-ATPase promoter. This model is particularly significant as it mimics the elevated IL-1β levels observed in human gastric cancer patients, providing insights into inflammation-driven gastric carcinogenesis.
- These transgenic mice develop spontaneous inflammation in the stomach, characterized by progressive infiltration of inflammatory cells and increased expression of pro-inflammatory cytokines. The chronic inflammatory environment leads to sequential changes in the gastric mucosa, including metaplasia, dysplasia, and eventually gastric cancer, closely resembling the human disease progression pattern.
- When exposed to Helicobacter infection, these mice show accelerated development of preneoplastic lesions compared to wild-type controls. The synergistic effect between IL-1β overexpression and bacterial infection provides a valuable tool for studying how inflammation and infection cooperate in gastric cancer development. This model is particularly useful for investigating the role of inflammatory mediators in cancer progression.
- A key feature of this model is its ability to demonstrate the direct link between chronic inflammation and cancer development. The constitutive expression of IL-1β in the stomach leads to activation of various signaling pathways involved in cell survival, proliferation, and angiogenesis. This helps researchers understand how sustained inflammatory signaling contributes to the transformation of normal gastric epithelium into cancer.
- The H/K-ATPase-IL-1β model has proven valuable for testing anti-inflammatory therapies and potential cancer preventive strategies. It allows researchers to evaluate interventions targeting the IL-1β pathway and other inflammatory mediators, offering insights into potential therapeutic approaches for inflammation-associated gastric cancer. The model continues to be essential for understanding the complex relationship between chronic inflammation and gastric carcinogenesis.
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