Epidemiology of Helicobacter Pylori Transmission

幽门螺杆菌传播的流行病学

基本信息

批准号：
8102528
负责人：
Julie Parsonnet
金额：
$ 17.6万
依托单位：
STANFORD UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2010
资助国家：
美国
起止时间：
2010-07-12 至 2012-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8102528
关键词：
Address Affect Aftercare Animal Model Antigens Area Biopsy California China Chronic Cirrhosis Colombia Community Surveys Complement Factor H Complex County Developed Countries Developing Countries Development Diagnostic Diarrhea Disease Disease Outcome Down-Regulation Economic Development Endoscopy Epidemiology Equilibrium Esophageal Adenocarcinoma Extinction (Psychology)Family Feces Funding Gastric Adenocarcinoma Gastric lymphoma Gastroenteritis Gastroesophageal reflux disease Helicobacter Helicobacter Infections Helicobacter pylori Helminths Hepatitis Viruses Household Human Immigrant Immune response Immune system Immunity Immunoglobulins Immunologic Epidemiology Immunologics Incidence Individual Infection Infectious Agent Inflammation Interferon Type II Intestines Iron deficiency anemia Joints Light Malignant neoplasm of liver Methodology Mycobacterium tuberculosis Organism Outcome Pathogenesis Patients Pattern Peptic Ulcer Peripheral Blood Mononuclear Cell Persons Phase Play Population Prevalence Production Purpura Pylorus Research Research Personnel Risk Risk Factors Sampling Signal Transduction Stimulus Stomach Tuberculosis Vaccines body system cell mediated immune response cytokine human disease latent infection malignant stomach neoplasm microbial pathogen programs protective effect response transmission process treatment effect vaccine development

项目摘要

Economic development has been accompanied by dramatic changes in the prevalence of some chronic infections. H. pylori, for example, is nearing extinction in industrialized countries. In developing countries, however, chronic infections remain common and act on the host simultaneously, resulting in competing signals to the immune system. In our prior submission, we identified protective effects of H. pylori on gastroenteritis incidence. This finding exemplifies the complex interactions that can occur among infectious agents in a single host to affect disease outcome. The objective of our current proposal is to better characterize how infections interact within humans. Specifically, we wish to see how host response to gastric infection with H. pylori varies in the setting of strong chronic inducers of Thl response (M. tuberculosis) or Th2 response (intestinal helminths). Specific aims are 1) to characterize the joint distribution of the three target pathogens in a defined population; 2) to characterize gastric and systemic immunologic profiles of mixed infections, and 3) to assess changes in these immunologic profiles after treatment of infection. In the setting of mixed infection, we speculate helminths cause down-regulation of cell-mediated immune responses to H. pylori whereas latent Mycobacterium tuberculosis (LTBI) upregulates the response. We further hypothesize that eradication of either helminths or LTBI reverses these effects. To be conducted in recent immigrants in Santa Clara county, the proposed research will have three parts. In Part 1, community surveys will be carried out and the distributions of infection in 1750 subjects will be evaluated. In Part 2, a subset of 200 subjects from phase one will undergo more extensive immunologic profiling to evaluate the effects of individualand co-infection on systemic cytokine arid immunoglobulin levels. In Part three, subjects who participated in Part II will undergo treatment of either helminths, latent tuberculosis infection or no treatment and changes in systemic immunologic outcomes will be assessed; in a subset of 75, immune responses to H. pylori in the stomach will also be assessed with endoscopy and biopsy. How humans respond to the spectrum of chronic infections that they harbor is a question of critical importance to vaccine development and to our understanding of the variability in manifestations of human disease. In addition to shedding light on why outcomes of H. pylori differ from person-to-person and from population-to-population, we hope this study will also expand the toolkit of immunoepidemiology for further studies in human populations.

经济发展伴随着一些慢性感染患病率的巨大变化。例如，幽门螺杆菌在工业化国家已接近灭绝。然而，在发展中国家，慢性病感染仍然很常见，并且同时作用于宿主，导致向免疫系统发出竞争信号。在我们之前提交的材料中，我们确定了幽门螺杆菌对胃肠炎发病率的保护作用。这一发现例证了单个宿主的感染因子之间可能发生复杂的相互作用，从而影响疾病的结果。这我们当前提案的目标是更好地描述感染在人类内部如何相互作用。具体来说，我们希望观察宿主对幽门螺杆菌胃部感染的反应在Thl强慢性诱导剂的情况下如何变化反应（结核分枝杆菌）或 Th2 反应（肠道蠕虫）。具体目标是 1) 表征联合三种目标病原体在特定人群中的分布； 2) 表征胃和全身免疫学混合感染的概况，3) 评估感染治疗后这些免疫学概况的变化。在在混合感染的情况下，我们推测蠕虫会导致细胞介导的幽门螺杆菌免疫反应下调。幽门螺杆菌，而潜伏结核分枝杆菌 (LTBI) 则上调反应。我们进一步假设根除蠕虫或 LTBI 可以逆转这些影响。将在圣克拉拉的新移民中进行县，拟议的研究将分为三个部分。第 1 部分将进行社区调查并将评估 1750 名受试者的感染分布。在第 2 部分中，第一阶段的 200 名受试者将进行更广泛的免疫学分析，以评估个体感染和合并感染对全身的影响细胞因子和免疫球蛋白水平。在第三部分中，参加第二部分的受试者将接受以下任一治疗蠕虫、潜伏性结核感染或不治疗以及全身免疫结果的变化将评估；在 75 人的子集中，还将通过内窥镜检查和评估胃中幽门螺杆菌的免疫反应活检。人类如何应对他们所携带的一系列慢性感染是一个至关重要的问题疫苗的开发以及我们对人类疾病表现变异性的理解。此外我们希望能够阐明为什么幽门螺杆菌的结果因人而异、因人群而异这项研究还将扩展免疫流行病学的工具包，以便在人群中进行进一步的研究。

项目成果

期刊论文数量（16）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Household transmission of gastroenteritis.

DOI：
10.3201/eid1107.040889
发表时间：
2005-07
期刊：
Emerging infectious diseases
影响因子：
11.8
作者：
Perry S;de la Luz Sanchez M;Hurst PK;Parsonnet J
通讯作者：
Parsonnet J

Gastroenteritis and transmission of Helicobacter pylori infection in households.

DOI：
10.3201/eid1211.060086
发表时间：
2006-11
期刊：
Emerging infectious diseases
影响因子：
11.8
作者：
Perry S;de la Luz Sanchez M;Yang S;Haggerty TD;Hurst P;Perez-Perez G;Parsonnet J
通讯作者：
Parsonnet J

Helicobacter pylori and risk of gastroenteritis.

幽门螺杆菌和胃肠炎的风险。

DOI：
10.1086/421705
发表时间：
2004
期刊：
The Journal of infectious diseases.
影响因子：
0
作者：
Perry,Sharon;Sanchez,Luz;Yang,Shufang;Haggerty,ThomasD;Hurst,Philip;Parsonnet,Julie
通讯作者：
Parsonnet,Julie

The immune response to tuberculosis infection in the setting of Helicobacter pylori and helminth infections.