Biomaterials that Promote Infection Immunity
促进感染免疫的生物材料
基本信息
- 批准号:8074519
- 负责人:
- 金额:$ 51.57万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2008
- 资助国家:美国
- 起止时间:2008-06-07 至 2013-05-31
- 项目状态:已结题
- 来源:
- 关键词:2-hydroxyethyl methacrylateAffectAirAmericanAmmoniumAnti-Infective AgentsAntibiotic TherapyAntibioticsAntibodiesAntibody FormationAntigen PresentationAntigen-Presenting CellsAntigensArtificial HeartArtificial cardiac pacemakerB-Cell ActivationB-LymphocytesBacteriaBacterial AdhesinsBindingBiocompatible MaterialsBiologicalBlood Vessel ProsthesisCD8B1 geneCardiovascular systemCathetersCause of DeathCellsCenters for Disease Control and Prevention (U.S.)Cerebrospinal fluid shunts procedureCessation of lifeChimeric ProteinsChlorhexidineCiprofloxacinCodeCommunitiesContact LensesControl GroupsCoupledCouplingDendritic CellsDevice RemovalDevicesDoseDrug FormulationsEngineeringEpitopesEscherichia coliExhibitsExposure toFCGR3B geneFibronectinsGeneric DrugsGenesGoalsGrowthHealedHealthHeart Valve ProsthesisHospitalsHumanHydrogelsImmune responseImmunityImmunizationImplantIn VitroIndwelling CatheterInfectionInflammatoryIntrauterine DevicesInvadedLeftLiquid substanceMHC Class I GenesMHC Class II GenesMechanicsMedicalMedical DeviceMemory B-LymphocyteMessenger RNAMethodsMicrobial BiofilmsModelingMonoclonal AntibodiesMusNosocomial InfectionsOcular ProsthesisOpsoninOrganismOrthopedicsParticulatePatientsPerformancePhagocytosisPharmaceutical PreparationsPolymersProsthesisRecombinantsResearch Project GrantsResidual stateSeriesSilverSkinStagingStaphylococcus epidermidisSurfaceSystemT cell responseT-LymphocyteTherapeuticTimeTransfectionUnited States National Institutes of HealthVaccinesVirulence Factorsantimicrobialbasecontrolled releasecostdesigndisorder preventionhealingimplantable deviceimplantationin vivokiller T cellkillingsmacrophagemeetingsmicrobialmonocytemonomernovelparticlepoly(2-hydroxyethyl methacrylate)-polyamine graft copolymerpreventprotein complexreceptorreceptor bindingresponsescaffoldstressorsuccesstraffickinguptakeurinaryvectorvector vaccineventricular assist device
项目摘要
DESCRIPTION (provided by applicant): Nosocomial infections are the fourth leading cause of death in the U.S. with >2 million cases annually (or ~10% of American hospital patients). About 60% of these infections are associated with an implanted medical device causing >$4.5 billion medical costs in 1992 and ~80,000 deaths annually. It is estimated that over 5 million artificial or prosthetic parts are implanted per annum in the U.S. alone. Our goal, with NIH support, is to engineer biomaterials that will solicit a short- and long-term immune response to specific bacterial colonization. For short-term immediate defense, model biomaterials will release fusion protein complexes - artificial opsonins - designed to enhance the coupling of invading bacteria to monocyte/macrophage (MO); thus promoting phagocytosis. For long-term protection, the biomaterial will transfect antigen-presenting cells (specifically dendritic cells - DCs) to produce T- and B-cell memory and antibody expression, and potentially stimulate direct native killer T-cell responses. PUBLIC HEALTH RELEVANCE: It is estimated that over 5 million artificial or prosthetic devices are implanted per annum in the U.S. alone. However, 70% of hospital-acquired infections are associated with implants or indwelling medical devices, with the case-to-fatality ratio between 5-50%. In this 5-yr NIH RO1 research grant, we will develop a novel class of biomaterials that promote healing while preventing bacterial colonization and subsequent infections.
描述(由申请人提供):医院感染是美国第四大死亡原因,每年有超过 200 万例病例(约占美国医院患者的 10%)。其中大约 60% 的感染与植入医疗设备有关,1992 年造成的医疗费用超过 45 亿美元,每年约有 8 万人死亡。据估计,仅在美国每年就有超过 500 万个人造或假肢被植入。在 NIH 的支持下,我们的目标是设计生物材料,以激发对特定细菌定植的短期和长期免疫反应。为了实现短期即时防御,模型生物材料将释放融合蛋白复合物——人工调理素——旨在增强入侵细菌与单核细胞/巨噬细胞(MO)的偶联;从而促进吞噬作用。为了实现长期保护,生物材料将转染抗原呈递细胞(特别是树突状细胞 - DC)以产生 T 细胞和 B 细胞记忆和抗体表达,并可能刺激直接的天然杀伤 T 细胞反应。公共卫生相关性:据估计,仅在美国每年就有超过 500 万个人工或假肢装置被植入。然而,70% 的医院获得性感染与植入物或留置医疗器械有关,病死率在 5-50% 之间。在这项为期 5 年的 NIH RO1 研究资助中,我们将开发一类新型生物材料,可促进愈合,同时防止细菌定植和随后的感染。
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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James D. Bryers其他文献
James D. Bryers的其他文献
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