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Project 3: Post-transcriptional regulation of innate immunity to Legionella pneumophila

项目3：嗜肺军团菌先天免疫的转录后调控

基本信息

批准号：
9977107
负责人：
RUSSELL E VANCE
金额：
$ 34.11万
依托单位：
UNIVERSITY OF CALIFORNIA BERKELEY
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-12-01 至 2021-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9977107
关键词：
Affect Amino Acids Animal Model Anti-Bacterial Agents Autophagocytosis Bacteria Bacterial Infections CRISPR/Cas technology Cell Line Cells Collaborations Complex Consumption Cytosol Data Dissection Equilibrium Family Gene Expression Profiling Genes Genetic Transcription Goals Growth Human IRF3 gene Immune response Infection Innate Immune Response Interferon Type I Knock-in Mouse Legionella pneumophila Legionnaires&apos Disease Listeria monocytogenes Mediating Metabolic Metabolism Mus Mycobacterium tuberculosis Natural Immunity Nutrient Outcome Pathogenesis Pathway interactions Phosphorylation Phosphotransferases Post-Transcriptional Regulation Program Research Project Grants Protein Biosynthesis Proteins Role STAT6 gene Technology Testing Therapeutic Intervention Transcription Process Type IV Secretion System Pathway Virulent cell growth cytokine expectation human morbidity human mortality in vivo mutant new technology new therapeutic target novel pathogen pathogenic bacteria response

项目摘要

Project Summary/Abstract (Project 3, Vance) Intracellular pathogens remain a significant global cause of human morbidity and mortality. The overall goal of this Program Project Grant is to characterize the host pathways that specifically detect and eliminate intracellular bacterial pathogens. Project 3 will contribute to this overall goal by focusing on the intracellular gram-negative bacterial pathogen Legionella pneumophila, the cause of Legionnaires' Disease in humans. As in previous iterations of this Program Project Grant, our core strategy is to compare the host responses induced by L. pneumophila to those induced by L. monocytogenes (Project 1) and M. tuberculosis (Project 2). Leveraging these comparisons allows us to identify pathogen-specific responses as well as universal responses induced by diverse intracellular bacterial pathogens. Three aims are proposed. In Aim 1, we test the hypothesis that postranscriptional responses downstream of the STING pathway are important in controlling intracellular bacterial infections. In Aim 2, we test the hypothesis that L. pneumophila specifically targets the mTORC1 pathway. We hypothesize that mTORC1 manipulation liberates host amino acids for bacterial consumption, but also contributes to innate immune responses to the bacterium. Lastly, in Aim 3, we take a broader approach and use comprehensive profiling technologies to identify novel post-transcriptional responses that regulate the host response to L. pneumophila. Our expectation is that by discovering novel host pathways that regulate intracellular bacterial growth and innate immunity, we will identify targets that can be exploited for therapeutic intervention.

项目摘要/摘要（项目3，万斯）