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Quorum Sensing in the Commensal Bacterium Bacteroides fragilis

脆弱拟杆菌中的群体感应

基本信息

批准号：
8254124
负责人：
Anisa Salim Ismail
金额：
$ 5.22万
依托单位：
PRINCETON UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2012
资助国家：
美国
起止时间：
2012-02-01 至 2014-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8254124
关键词：
Anti-Inflammatory Agents Anti-inflammatory Automobile Driving Bacteria Bacteroides fragilis Behavior Biochemical Biological Assay Cell Communication Cells Chemicals Chronic Disease Cloning Colitis Communication Complex Crohn&apos s disease Detection Development Disease Environment Epithelial Cells Escherichia coli Eukaryota Eukaryotic Cell Experimental Animal Model Future Genes Genetic Goals Health Homeostasis Human Immune Immune system Indigenous Infection prevention Inflammatory Bowel Diseases Inflammatory Response Intestines Invaded Lead Mammals Microbe Microbial Biofilms Modeling Molecular Mutagenesis Patients Phenotype Play Polysaccharides Process Prokaryotic Cells Regulation Reporter Role Salmonella typhimurium Shapes Signal Transduction Signaling Molecule Staging Symbiosis Therapeutic Work commensal microbes gut microflora homoserine lactone improved in vivo insight intercellular communication intestinal epithelium member microbial microbial host quorum sensing response trait

项目摘要

Quorum sensing in the commensal bacterium Bacteroides fragilis Intestinal epithelial cells provide the crucial interface (400 m[2]) between mammalian hosts and a vast consortium of microbial partners. Yet, little is known about the mechanisms regulating our beneficial relations with commensal bacteria. In a process called quorum sensing, bacteria communicate using chemical signal molecules called autoinducers. Quorum sensing allows bacteria to synchronize collective behaviors such as polysaccharide secretion and biofilm formation, hallmark traits deployed by commensal bacteria in the mammalian gut environment. The fact that bacteria and mammalian intestinal cells are in constant contact with one another, combined with the universal use of intercellular communication in prokaryotes and eukaryotes, has led me to speculate that bacteria- and/or mammalian-secreted signals are involved in maintaining homeostasis via intra- and inter-kingdom communication. I will investigate these ideas by studying Bacteroides fragilis-eukaryotic cell interactions. B. fragilis is a prominent member of the normal gut microflora that plays a vital role in maintaining intestinal health by directing host anti-inflammatory responses. However, the mechanisms underlying these interactions are not known. The goals of this proposal are to investigate how resident gut bacteria influence intestinal health through quorum sensing behaviors, to characterize quorum sensing factors directing collective behaviors in B. fragilis, and to define how the host immune system controls B. fragilis quorum sensing.

共生细菌脆弱拟杆菌中的群体感应肠上皮细胞在哺乳动物宿主和大量微生物伙伴之间提供了至关重要的界面（400 m[2]）。然而，人们对调节我们与共生细菌的有益关系的机制知之甚少。在称为群体感应的过程中，细菌使用称为自诱导剂的化学信号分子进行交流。群体感应使细菌能够同步集体行为，例如多糖分泌和生物膜形成，这是哺乳动物肠道环境中共生细菌的标志性特征。细菌和哺乳动物肠细胞彼此持续接触这一事实，加上原核生物和真核生物中细胞间通讯的普遍使用，使我推测细菌和/或哺乳动物分泌的信号通过界内和界间通讯参与维持体内平衡。我将通过研究脆弱拟杆菌与真核细胞的相互作用来研究这些想法。脆弱拟杆菌是正常肠道菌群的重要成员，通过指导宿主抗炎反应在维持肠道健康方面发挥着至关重要的作用。然而，这些相互作用背后的机制尚不清楚。该提案的目标是研究常驻肠道细菌如何通过群体感应行为影响肠道健康，表征指导脆弱拟杆菌集体行为的群体感应因素，并确定宿主免疫系统如何控制脆弱拟杆菌群体感应。