作者: Hidekazu Suzuki , Toshifumi Hibi
DOI: 10.3164/JCBN.39.56
关键词: Gastric mucosa 、 Intracellular signal transduction 、 Immunology 、 Atrophic gastritis 、 Gastric Infection 、 Helicobacter pylori 、 Internal medicine 、 Intestinal metaplasia 、 Chronic gastritis 、 Gastritis 、 Biology 、 Gastroenterology
摘要: Helicobacter pylori (H. pylori) is a spiral-shaped, Gram-negative rod, which induces the infiltration to gastric mucosa by neutrophils, macrophages, and T B lymphocytes; however, this immune inflammatory response cannot completely clear bacterial infection, leaves host prone complications resulting from persistent inflammation. Resultantly, H. infection causes chronic inflammation, accumulation of reactive oxygen species, oxidative DNA damage in mucosa. Recent studies reveal that injects proteins into cytosol cell via type IV injection system regulates intracellular signal transduction [1, 2]. This mechanism provides novel means resolving how survives acidic environment human stomach. During infections, gastritis may remain asymptomatic or evolve more severe diseases, such as peptic ulcer disease atrophic gastritis. In addition, with increases risk developing cancer mucosa-associated lymphoid tissue lymphoma. Various gastritis, ulcers, intestinal metaplasia, cancer, can be appropriately developed inoculating bacteria Mongolian gerbils [3]. successful eradication useful preventive approach against [4]. review focuses on aspects pylori-associated mucosal lesion formation.