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C-di-AMP signaling in S. aureus

金黄色葡萄球菌中的 C-di-AMP 信号传导

基本信息

批准号：
10089215
负责人：
Joshua Woodward
金额：
$ 54.86万
依托单位：
UNIVERSITY OF WASHINGTON
依托单位国家：
美国
项目类别：
财政年份：
2019
资助国家：
美国
起止时间：
2019-02-01 至 2024-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10089215
关键词：
Adolescent Antibiotic Resistance Antibiotic Therapy Antibiotic susceptibility Bacteria Bacterial Infections Bacterial Physiology Binding Biochemical Cells Cessation of life Chronic Cladribine Clinical Cystic Fibrosis Disease Disease Progression Enzymes Exhibits Gammaproteobacteria Gene Expression Regulation Growth Human Genetics Immune System Diseases Immunity Infection Infectious Skin Diseases Inflammation Inflammatory Influenza Interferon-beta Interferons Laboratories Link Longitudinal cohort Lung infections Mediating Mediator of activation protein Metabolism Modeling Molecular Monitor Morbidity - disease rate Multi-Drug Resistance Mus Nucleotides Organism Outcome Pathogenesis Pathologic Pathology Periodicity Phenotype Physiology Pneumonia Predisposition Process Production Proteins Proteobacteria Pseudomonas aeruginosa Pulmonary Fibrosis Role Second Messenger Systems Signal Transduction Signaling Molecule Skin Tissue Soft Tissue Infections Staphylococcus aureus Staphylococcus aureus infection Study models Surgical Wound Infection Testing Therapeutic Intervention Thymidine Tissues Variant Virulence Wound Infection acute infection base cell behavior chronic infection chronic wound co-infection cystic fibrosis patients environmental change genetic association human disease human morbidity human mortality immune activation in vivo insight mortality new therapeutic target novel pulmonary function decline receptor response soft tissue superinfection thymidylate kinase tissue culture

项目摘要

Abstract Staphylococcus aureus is a leading cause of human morbidity and mortality, causing infection of the skin and soft tissues, post-surgical wounds, and lung infection among influenza and cystic fibrosis patients. Widespread multi-drug resistance has made eradication of S. aureus increasingly challenging, necessitating a deeper understanding of the physiology and pathogenesis associated with these organisms. A key aspect of bacterial survival and adaptation to altered environmental conditions is the ability to rapidly alter cellular behavior through second messenger signal transduction. C-di-AMP has recently emerged as a key regulator of bacterial physiology, pathogenesis, and immune activation. In the context of S. aureus, we believe that c- di-AMP produced by S. aureus has three important roles; (i) as a signaling molecule that mediates S. aureus metabolism and antibiotic resistance, (ii) as a bacterial PAMP that promotes pathological inflammation and host susceptibility to bacterial infection, and (iii) as a mediator of inter-bacterial signaling that alters the outcome of co-infections. Findings from these studies may have significant impacts on the course of antibiotic therapy during S. aureus infection and may uncover a novel target to eradicate recalcitrant S. aureus and the inflammation itpromotes.

摘要