Chronic inflammation and long-lasting changes in the gastric mucosa after Helicobacter pylori infection involved in gastric cancer

Helicobacter pylori (H. pylori) infects approximately half of the world’s population, as one of the most common chronic infections. H. pylori infection has been widely recognized as a major risk factor for gastric cancer (GC). Eradication treatment is considered to abolish the inflammatory response and prevent progression to GC. However, only 1–3% of H. pylori-infected patients develop GC, whereas GC can occur even after eradicating H. pylori. In addition, the incidence of GC following H. pylori infection is significantly higher compared to the gross incidence induced by all causes, although eradicating H. pylori reduces the risk of developing GC. Therefore, it is reasonable to hypothesize that H. pylori infection results in changes that persist even after its eradication. Several of these changes may not be reversible within a short time, including the status of inflammation, the dysfunction of immunity and apoptosis, mitochondrial changes, aging and gastric dysbacteriosis. The present review article aimed to discuss these potential long-lasting changes induced by H. pylori infection that may follow the eradication of H. pylori and contribute to the development of GC.