Helicobacter pylori (H. pylori) infection is a causal factor of gastric cancer. Among the cytokines secreted during this infection, IL-1β is highly associated with promotion and progression of gastric cancer. On the therapeutic front, eradication of H. pylori was thought to be efficient to restore gastric homeostasis. However, successful H. pylori eradication in patients with advanced stages (intestinal metaplasia) failed to diminish inflammation that is due to heightened Th17 response and elevated IL-1β levels. In fact, association between these two components was established, suggesting that IL-1β is a critical target in these cases. In this review, we will discuss the functional relevance of IL-1β in advanced H. pylori infection and how its targeting may bring clinical benefit.
Keywords: Helicobacter pylori; IL-1β; gastric cancer; inflammation.
Helicobacter pylori (H. pylori) infection is a causal factor of gastric cancer. This disease is strongly associated to an inflammatory factor (interleukin 1β). On the therapeutic front, eradication of H. pylori was thought to be efficient to restore gastric comfort. However, successful H. pylori eradication in patients with advanced stages of this infection failed to diminish inflammation, due to the inflammatory factor cited preciously, thereby exacerbating gastric tissue damage. In this review, we will discuss the functional relevance of IL-1β in advanced H. pylori infection and how its targeting may bring clinical benefit.