Immune Response to H. Pylori Infection

宿主免疫应答在确定慢性感染的疾病表现中起着关键作用。 免疫应答不足可能无法控制感染，尽管在其他情况下， 反应可能是组织损伤和疾病的原因。大多数慢性感染患者 可能被一种以上的微生物感染;然而，多种活性物质之间的相互作用 感染尚不清楚，对疾病结果的影响也不清楚。慢性感染，如螺杆菌 幽门螺杆菌是世界范围内相当大的发病率和死亡率的原因。与急性感染不同， “一种微生物一种疾病”的概念可以应用，由慢性感染性微生物引起的疾病更多 可能代表感染微生物与多种宿主和环境之间的相互作用 包括与其他感染因子的相互作用[1]。 我们和其他人已经证明了在选定的哥伦比亚人群中蠕虫病的高发病率， 尤其是儿童（2，3）。我们的初步研究[2]表明，对H.幽门螺杆菌感染 在低风险的沿海人口主要是Th 2型，它可能与肠道 蠕虫病这一观察结果与我们的报告一致，即肠道蠕虫病减少了胃肠道疾病的发生。 萎缩，一种癌前病变，在C57 BL/6小鼠幽门螺杆菌胃炎模型中[4]。我们最近的研究 在沙鼠中显示H.幽门螺杆菌相关的沙土鼠癌前病变的衰减 Brugia sp.也支持这一假说。 在这些拟议的研究中，我们将检验这一假设，即胃癌的进展不受 仅受H.幽门（即，H.幽门螺杆菌菌株来自高胃肠道感染地区的患者 癌症风险区域导致更多的亚硝化和氧化损伤。幽门螺杆菌菌株与低位胃癌的关系 风险区域）[5]，但也可能是由于寄生虫的并发感染，寄生虫可调节全身免疫 应答和Th 1/Th 2胃细胞因子谱。 相关性（见说明）： 宿主免疫应答在确定个体如何应答慢性感染中是重要的。 幽门螺杆菌引起的胃病这些免疫反应在预测为什么 某些H.幽门螺杆菌感染会导致胃癌。

The host immune response plays a critical role in determining disease manifestations of chronic infections. Inadequate immune response may fail to control infection, although in other cases the specific immune response may be the cause of tissue damage and disease. The majority of patients with chronic infections are likely to be infected by more than one organism; however, the interaction between multiple active infections is not known, nor is the impact on disease outcome clear. Chronic infections such as Helicobacter pylori are the cause of considerable morbidity and mortality, worldwide. Unlike acute infections, where the "one microbe- one disease" concept can be applied, disease caused by chronic infectious organisms more likely represents interactions between the infecting organism(s) and a multitude of hosts and environmental factors including interaction with other infectious agents [1]. We and others have demonstrated the high incidence of helminthiasis in select Colombian populations, particularly children (2,3]. Our preliminary studies [2] suggest that the immune response to H. pylori infection in the low-risk coastal population is predominantly type Th2 and that it may be related to intestinal helminthiasis. This observation is consistent with our report that intestinal helminthiasis reduced gastric atrophy, a premalignant lesion, in the C57BL/6 mouse model of Helicobacter gastritis [4]. Our recent studies in gerbils demonstrating an H. pylori-associated attenuation of premalignant lesions in gerbils coinfected with Brugia sp. also support this hypothesis. In these proposed studies, we will test the hypothesis that progression to gastric cancer is influenced not only by the genotype of H. pylori (i.e., the ability of H. pylori strains from patients in regions of high gastric cancer risk areas to cause more nitrosative and oxidative damage vs. H. pylori strains in low gastric cancer risk areas) [5], but also by concun-ent infection with parasites which can modulate systemic immune responses and the Th1/Th2 gastric cytokine profile. RELEVANCE (See Instructions): The host immune response is important in determining how an individual responds to the chronic infection in the stomach caused by Helicobacter pylori. These immune responses play a critical role in predicting why certain patients with H. pylori infection develop gastric cancer.