ROLE OF H PYLORI OUTER MEMBRANE PROTEINS IN COLONIZATION AND HOST RESPONSE
幽门螺杆菌外膜蛋白在定植和宿主反应中的作用
基本信息
- 批准号:8357312
- 负责人:
- 金额:$ 7.56万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2011
- 资助国家:美国
- 起止时间:2011-05-01 至 2012-04-30
- 项目状态:已结题
- 来源:
- 关键词:ABO blood group systemAddressAffinityBacterial AdhesinsBindingBlood Group AntigensCaliforniaChronicClinicalCodeDinucleoside PhosphatesDiseaseEpitheliumEventFamilyFundingGastritisGene ConversionGenesGenomeGrantHealthHelicobacter InfectionsHelicobacter pyloriHumanImmune responseImmunityIndividualInfectionInflammationMacacaMacaca mulattaMediatingMembrane ProteinsModificationMusNational Center for Research ResourcesPatientsPeptic UlcerPlayPrimatesPrincipal InvestigatorProteinsResearchResearch InfrastructureResourcesRoleSourceStomachSurfaceTranslational ResearchUnited States National Institutes of HealthVariantadaptive immunityclinically relevantcostmalignant stomach neoplasmpathogenprotein expressionprotein profilingvaccine candidate
项目摘要
This subproject is one of many research subprojects utilizing the resources
provided by a Center grant funded by NIH/NCRR. Primary support for the subproject
and the subproject's principal investigator may have been provided by other sources,
including other NIH sources. The Total Cost listed for the subproject likely
represents the estimated amount of Center infrastructure utilized by the subproject,
not direct funding provided by the NCRR grant to the subproject or subproject staff.
Helicobacter pylori commonly infects the stomach, where it causes inflammation (gastritis) in all individuals and peptic ulcer disease or gastric cancer in some. H. pylori attachment to the gastric epithelium is mediated by a large family of outer membrane proteins (OMPs), the best studied of which is BabA, the Lewis b (Leb)/ABO blood group binding adhesin. BabA is clinically relevant because patients infected with strains that express it are more likely to develop peptic ulcer or gastric cancer. A closely related protein, BabB, shows extensive homology with BabA, but its function is unknown. We recently showed that H. pylori strains recovered from experimentally infected macaques had lost expression of BabA. In some cases the babA gene was replaced by babB (an apparent gene conversion event) and in other cases the babA gene was not expressed due to alteration in the number of dinucleotide CT repeats in the 5' coding region. Strains lacking BabA expression did not adhere to the Leb blood group antigen that is expressed on rhesus gastric epithelium. Analysis of human clinical strains showed that many patients are infected with variants of H. pylori whose OMP profile resembles that seen in macaques. Since BabA expression is also lost during experimental infection of both wild type and Rag-/- mice, evasion of adaptive immunity is probably not playing a role. We hypothesize that modifications in H. pylori OMP expression represents a remodeling of the bacterial surface so as to avoid innate host immunity and promote attachment to the gastric epithelium. Four Specific Aims are proposed to address this hypothesis. Aim 1 will determine the effect of BabA and BabB on host response and modulation of OMP expression during H. pylori infection of rhesus macaques. In Aim 2 we will determine the competitive effect of BabA and BabB on H. pylori colonization of rhesus macaques. Aim 3 will examine the role of affinity of BabA binding to Leb on the expression of BabA. In Aim 4 we will characterize the role of BabB in H. pylori attachment. These studies of BabA and BabB will contribute to ongoing translational research that seek to investigate the use of BabA and BabB as vaccine candidates, and also may have broad implications for the role of genome diversity in promoting chronic infection with H. pylori. PUBLIC HEALTH RELEVANCE: Helicobacter pylori is a bacterial pathogen that commonly infects the human stomach and sometimes causes peptic ulcers or gastric cancer. One factor that determines whether infection causes disease, or just asymptomatic colonization, is the particular profile of surface proteins that mediate attachment to the gastric epithelium. This project seeks to understand some of the factors that determine the expression of these surface proteins in H. pylori.
这个子项目是利用这些资源的众多研究子项目之一
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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JAY V. SOLNICK其他文献
JAY V. SOLNICK的其他文献
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{{ truncateString('JAY V. SOLNICK', 18)}}的其他基金
Functional Plasticity in the Helicobacter pylori Type IV Secretion System
幽门螺杆菌 IV 型分泌系统的功能可塑性
- 批准号:
8743130 - 财政年份:2014
- 资助金额:
$ 7.56万 - 项目类别:
Functional Plasticity in the Helicobacter pylori Type IV Secretion System
幽门螺杆菌 IV 型分泌系统的功能可塑性
- 批准号:
8889192 - 财政年份:2014
- 资助金额:
$ 7.56万 - 项目类别:
Functional Plasticity in the Helicobacter pylori Type IV Secretion System
幽门螺杆菌 IV 型分泌系统的功能可塑性
- 批准号:
9301473 - 财政年份:2014
- 资助金额:
$ 7.56万 - 项目类别:
Functional Plasticity in the Helicobacter pylori Type IV Secretion System
幽门螺杆菌 IV 型分泌系统的功能可塑性
- 批准号:
9094671 - 财政年份:2014
- 资助金额:
$ 7.56万 - 项目类别:
HELICOBACTER PYLORI AND THE GASTRIC MICROBIAL COMMUNITY IN RHESUS MACAQUES
恒河猴中的幽门螺杆菌和胃微生物群落
- 批准号:
8357316 - 财政年份:2011
- 资助金额:
$ 7.56万 - 项目类别:
DEFENSIN GENE COPY NUMBER AND MUCOSAL INNATE IMMUNITY
防御素基因拷贝数和粘膜先天免疫
- 批准号:
8357354 - 财政年份:2011
- 资助金额:
$ 7.56万 - 项目类别:
PREVENTION OF ACTIVE TUBERCULOSIS BY INFECTION WITH H PYLORI
通过幽门螺杆菌感染预防活动性结核病
- 批准号:
8357314 - 财政年份:2011
- 资助金额:
$ 7.56万 - 项目类别:
MODULATION OF OUTER MEMBRANE PROTEIN EXPRESSION IN HELICOBACTER PYLORI
幽门螺杆菌外膜蛋白表达的调节
- 批准号:
8357315 - 财政年份:2011
- 资助金额:
$ 7.56万 - 项目类别:
GENE EXPRESSION DURING H PYLORI-HOST INTERACTION
幽门螺杆菌-宿主相互作用期间的基因表达
- 批准号:
8357261 - 财政年份:2011
- 资助金额:
$ 7.56万 - 项目类别:
PROPHYLACTIC AND THERAPEUTIC IMMUNIZATION AGAINST H PYLORI IN RHESUS MACAQUES
恒河猴中针对幽门螺杆菌的预防性和治疗性免疫
- 批准号:
8357306 - 财政年份:2011
- 资助金额:
$ 7.56万 - 项目类别:
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