Sánchez-Zauco Norma Angélica, Giono-Cerezo Silvia, Maldonado-Bernal Carmen
Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, México, DF, México.
Salud Publica Mex. 2010 Sep-Oct;52(5):447-54. doi: 10.1590/s0036-36342010000500012.
Helicobacter pylori colonize the gastric epithelial, most infected people are asymptomatic, 10 to 20% develop atrophic gastritis, peptic ulcer and less than 3% gastric cancer. These diseases are determined by the relationship between virulence factors of bacteria, host factors such as, genetic predisposition, and immune response. The innate immune response mainly represented by Toll-like receptors and Nod-like receptors that recognize their specific ligands, activate transcription factors as NF-kB, AP-1, CREB-1, inducing production of inflammatory cytokines such as IL -8, IL-12, IL-6, IL-1β, IL-18, TNF-α and IL-10. Chronic inflammation promotes gastric morphological changes, prevents apoptosis and allows angiogenesis generating neoplasic lesions and cancer. The aim of this review is to analyze the mechanisms proposed to date of the innate and adaptative immune response involved in H. pylori infection; remarking the mechanisms related in the elimination or persistence.
幽门螺杆菌定殖于胃上皮，大多数感染者无症状，10%至20%会发展为萎缩性胃炎、消化性溃疡，不到3%会发展为胃癌。这些疾病由细菌毒力因子、宿主因素（如遗传易感性）和免疫反应之间的关系决定。固有免疫反应主要由识别其特定配体的Toll样受体和Nod样受体介导，激活转录因子如NF-κB、AP-1、CREB-1，诱导产生炎性细胞因子如IL-8、IL-12、IL-6、IL-1β、IL-18、TNF-α和IL-10。慢性炎症促进胃形态改变，阻止细胞凋亡并促进血管生成，从而产生肿瘤性病变和癌症。本综述的目的是分析迄今为止提出的参与幽门螺杆菌感染的固有免疫和适应性免疫反应机制；阐述与清除或持续存在相关的机制。
