认识幽门螺杆菌__培训课件.pptVIP

胃癌在全世界范围内是发病率最高的癌症之一 世界卫生组织癌控项目统计数据， 全球每年死于癌症的患者高达700万 死于胃癌的患者占了70万 胃癌发病率男性占第二位，女性占第四位 东亚国家（日本、朝鲜、韩国、中国）是胃癌高发地区 胃癌是我国的第二大常见肿瘤 好发年龄50岁以上 每年新增46万人，死亡人数为每年45万 根据世界卫生组织资料，2010年中国胃癌 病人占全球的47%。 Hp感染是胃癌的始发因素 幽门螺杆菌感染使患胃癌的危险增加了2.7~12倍，没有幽门螺杆菌感染，至少有35%~89%的胃癌不会发生 自儿童期控制Hp的感染，不仅可预防治疗良性上消化道疾病，也可降低胃癌的发生率 1994 年世界卫生组织( WHO) 已将Hp 列为第一类致癌因子， 已经确定根除 Hp 感染解决胃炎 可以治愈溃疡并阻止胃癌的发展 幽门螺杆菌具有很强的活性与繁殖能力，是一种严重影响公众健康的细菌 简单的检查、简单的治疗能够根除幽门螺杆菌 * H. pylori induces proinflammatory responses in epithelial cells by 2 pathways. H. pylori–induced proinflammatory responses are dependent on the presence in H. pylori of a functional type IV secretion system (T4SS), which delivers effector molecules, such as cell wall peptidoglycan (PGN) and the protein CagA, to epithelial cells. The precise mechanisms by which the H. pylori T4SS mediates effector delivery to host cells are, however, presently unknown. (i) Recognition of H. pylori PGN by the cytosolic host defense molecule NOD1 leads to NF-kB activation. On the basis of studies with Shigella flexneri, it is likely that NOD1 activates NF-kB via caspase-recruitment domain (CARD)–CARD interactions with receptor-interacting serine-threonine kinase (RICK; also known as RIP2). Activated NF-kB complexes translocate to the nucleus, where they upregulate expression of genes encoding the proinflammatory chemokines IL-8 and CXC-chemokine ligand 2 (CXCL2; also known as MIP2) and the antimicrobial peptide human b-defensin-2 (hBD-2). (ii) CagA translocation into epithelial cells by certain H. pylori strains able to induce high levels of IL-8 is also accompanied by the induction of an inflammatory response. Tyrosine phosphorylation of EPIYA motifs on CagA triggers a signaling cascade that involves the Ras-dependent kinases ERK1 and ERK2, leading to activation of the transcription factors NF-kB and activator protein-1 (AP-1) and, ultimately, IL-8 production by host cells. Courtesy of R. Ferrero (Monash University, Clayton, Victoria, Aus