Abstract
Helicobacter pylori (H. pylori) is a spiral-shaped, Gram-negative rod, which induces the infiltration to the gastric mucosa by neutrophils, macrophages, and T and B lymphocytes; however, this immune and inflammatory response cannot completely clear the bacterial infection, and leaves the host prone to complications resulting from persistent inflammation. Resultantly, H. pylori infection causes chronic inflammation, accumulation of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. Recent studies reveal that H. pylori injects bacterial proteins into the cytosol of the gastric host cell via the type IV injection system and regulates the intracellular signal transduction [1, 2]. This mechanism provides a novel means of resolving how H. pylori survives in the acidic environment of the human stomach. During persistent gastric infections, chronic gastritis may remain asymptomatic or may evolve into more severe diseases, such as peptic ulcer disease or atrophic gastritis. In addition, infection with H. pylori increases the risk of developing gastric cancer and mucosa-associated lymphoid tissue lymphoma. Various gastric diseases, such as gastritis, ulcers, intestinal metaplasia, and gastric cancer, can be appropriately developed by inoculating this bacteria into Mongolian gerbils [3]. In addition, the successful eradication of H. pylori is useful as a preventive approach against gastric cancer [4]. This review focuses on the aspects of the oxidative mechanism in the H. pylori-associated gastric mucosal lesion formation.
