Multi-omic Studies of Local and Systemic Immune Dysregulation in Rosacea
红斑痤疮局部和全身免疫失调的多组学研究
基本信息
- 批准号:10590784
- 负责人:
- 金额:$ 16.99万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2023
- 资助国家:美国
- 起止时间:2023-02-06 至 2028-01-31
- 项目状态:未结题
- 来源:
- 关键词:Advanced DevelopmentAffectAtherosclerosisBioinformaticsBiological AssayBiological Response ModifiersBiometryBloodBlood VesselsCellsCirculationClinical TrialsCommunicationComplexComputational BiologyCore FacilityCountryDataDevelopmentDiseaseEarly DiagnosisEducational workshopEnvironmentEpidemiologyEpitheliumEtiologyExclusionExpression ProfilingGenetic TranscriptionGoalsGrantHealthHomeostasisHuman Subject ResearchIL17 geneImmuneImmune responseInflammatoryInflammatory Bowel DiseasesInnate Immune ResponseInnate Immune SystemInstitutionInvestigationIsraelKininogenaseLinkMediatingMedical centerMentorsMicrobeMolecularMultiomic DataOutcomePathogenesisPathway interactionsPatientsPeptidesPersonsPhysiciansPreventionPrincipal InvestigatorProteomeProteomicsProtocols documentationPsoriasisPublic Health SchoolsRegulator GenesResearchRoleRosaceaScientistSerine ProteaseSerumShotgunsSignal PathwaySignal TransductionSkinStimulusSystemic diseaseTLR1 geneTLR2 geneTNF geneTeaching HospitalsTestingTherapeuticTrainingTranscriptional ActivationUnited StatesWhole BloodWritingburden of illnesscardiovascular risk factorcareercareer developmentcathelicidincathelicidin antimicrobial peptidecommensal microbescomorbiditycytokinedata integrationdysbiosisexperiencehost microbiotaimmune activationimprovedinsightinterleukin-22medical schoolsmetagenomic sequencingmicrobialmicrobiomemicrobiotamultidisciplinarymultiple omicsnew therapeutic targetnovelpersonalized strategiesprogramsprotein expressionrRNA Genesrecruitresearch and developmentresponseskin disorderskin microbiomeskin microbiotatherapeutic targettranscriptometranscriptome sequencingtranscriptomics
项目摘要
Project Summary/Abstract
Our research proposes to elucidate local and systemic immune dysregulation in rosacea with the long-term goals
of developing novel preventative and therapeutic targets and improving overall health outcomes for rosacea
patients. Rosacea is a common inflammatory skin disease with unclear etiology affecting over 14 million people
in the United States alone.1 Toll-like receptor 2 (TLR2) is a microbe-sensing mechanism that maintains immune
homeostasis in the skin through communication with commensal microbes.2-4 Therefore, we suspect that
understanding the skin microbiota-host interaction is critical to elucidating the pathogenesis of rosacea. Moreover,
the immune dysregulation in rosacea does not appear to be localized to the skin. There is a growing body of
epidemiological evidence demonstrating that rosacea is associated with a wide range of systemic co-
morbidities.40-51 Thus, it is also important to elucidate potential systemic immune dysregulation that can explain
the overall disease burden in rosacea patients. Aim 1: We aim to test the hypothesis that skin dysbiosis induces
transcription and expression of the components of the innate immune response implicated in the pathogenesis
of rosacea. To that end, we will perform multi-omics data integration of the microbiome, transcriptome, and
proteome from rosacea skin in order to delineate the microbiota-host interaction. Aim 2: We aim to test the
hypothesis that there is shared immune dysregulation between the skin and systemic circulation that can explain
the burden of systemic co-morbidities in rosacea patients. To that end, we will perform multi-omics data
integration of the transcriptome and proteome from the skin and blood/serum in order to characterize shared
molecular pathways. Dr. McGee’s career goal is to become a physician scientist with the unique expertise to
apply multi-omics, data-driven, personalized strategies to treat inflammatory skin diseases and their associated
systemic co-morbidities. To achieve this goal, she will undertake a combination of formalized coursework,
workshops, and hands-on training in bioinformatics, computational biology, human subjects research, and
clinical trials. She will also engage in career development activities by participating in a grant writing course and
a K-R transition program. Dr. McGee’s research and career development will be guided by a mentoring team
with several decades of combined experience in successfully transitioning their mentees to research
independence. Dr. McGee’s training will take place at two prominent academic institutions: 1) Beth Israel
Deaconess Medical Center, a major teaching hospital of Harvard Medical School which supports ~250 principal
investigators and offers 16 institutional and 12 departmental core facilities, and 2) Harvard T.H. Chan School of
Public Health, which hosts the consistently ranked #1 biostatistics program in the country and supports
computational research initiatives to answer multidisciplinary questions.
项目摘要/摘要
我们的研究旨在阐明酒渣鼻局部和全身免疫失调的长期目标。
开发新的预防和治疗目标并改善酒渣鼻的整体健康结局
病人。酒渣鼻是一种常见的炎症性皮肤病,病因不明,影响1400多万人。
在美国,Toll样受体2(TLR2)是一种维持免疫的微生物传感机制
通过与共生微生物的交流在皮肤中保持动态平衡。2-4因此,我们怀疑
了解皮肤微生物区系与宿主的相互作用对于阐明酒渣鼻的发病机制至关重要。此外,
酒渣鼻的免疫失调似乎并不局限于皮肤。有越来越多的
流行病学证据表明,酒渣鼻与广泛的系统性红斑狼疮有关。
因此,阐明潜在的全身性免疫失调也很重要,这可以解释
酒渣鼻患者的总体疾病负担。目的1:我们的目标是检验皮肤生物失调引起的假说
与发病有关的先天免疫反应成分的转录和表达
酒渣鼻。为此,我们将对微生物组、转录组和
从酒渣鼻皮肤中提取蛋白质组,以描述微生物区系与宿主之间的相互作用。目标2:我们的目标是测试
假设皮肤和体循环之间存在共同的免疫失调,这可以解释
酒渣鼻患者全身合并症的负担。为此,我们将进行多组学数据
从皮肤和血液/血清中整合转录组和蛋白质组以表征共享
分子途径。McGee博士的职业目标是成为一名具有独特专业知识的内科科学家
应用多组学、数据驱动、个性化策略来治疗炎症性皮肤病及其相关疾病
系统性共病。为了实现这一目标,她将进行一系列正式的课程作业,
生物信息学、计算生物学、人体研究和实践方面的研讨会和实践培训
临床试验。她还将参与职业发展活动,参加一个赠款撰写课程和
一个K-R过渡计划。McGee博士的研究和职业发展将由一个指导团队指导
在成功地将他们的学员过渡到研究方面,拥有几十年的综合经验
独立。麦基博士的培训将在两所著名的学术机构进行:1)贝丝·伊斯雷尔
女执事医疗中心,哈佛医学院的一家主要教学医院,支持约250名校长
研究人员,并提供16个机构和12个部门的核心设施,以及2)哈佛大学陈T.H.学院
公共卫生,该机构一直是全国排名第一的生物统计学项目的主持人,并支持
计算研究计划,以回答多学科问题。
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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Jean Suh McGee其他文献
Jean Suh McGee的其他文献
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{{ truncateString('Jean Suh McGee', 18)}}的其他基金
The role of Rif1p preferential elongation of short telomeres
Rif1p优先延长短端粒的作用
- 批准号:
8197823 - 财政年份:2009
- 资助金额:
$ 16.99万 - 项目类别:
The role of Rif1p preferential elongation of short telomeres
Rif1p优先延长短端粒的作用
- 批准号:
8192374 - 财政年份:2009
- 资助金额:
$ 16.99万 - 项目类别:
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