{"title":"细胞应激蛋白作为细菌-宿主相互作用的调节剂。","authors":"Brian Henderson","doi":"10.1002/9780470754030.ch11","DOIUrl":null,"url":null,"abstract":"<p><p>Multicellular organisms exist in dynamic equilibrium with bacterial populations, either in the form of the microbiota of the organism or as pathogens. A challenge to 21st century systems biology is to determine the networks of interactions that exist between the prokaryotic and eukaryotic components of multicellular organisms. Bacterial colonization is stressful for both the prokaryotic and eukaryotic components of an organism and it is emerging that the cell stress proteins (CSPs) of both bacteria and host play roles in the interaction between both Kingdoms. In addition to acting intracellularly to fold proteins, it is being established that CSPs have a wide range of moonlighting functions that are relevant to controlling bacterial colonization. Thus host CSPs can act as cell surface receptors to bind bacteria or to respond to their components. Host CSPs are also secreted into the extracellular fluid where they modulate leukocyte function, potentially to activate antibacterial defences. Bacteria, in turn, have evolved CSPs with adhesive properties for the host. Bacterial CSPs can also modulate host leukocyte function and can induce cellular apoptosis. In insects, endosymbiotic bacteria provide bacterial CSPs which are utilised by the host. Bacterial CSPs have also been shown to be antibacterial targets. These findings establish a range of roles for CSPs in bacteria-host interactions.</p>","PeriodicalId":19323,"journal":{"name":"Novartis Foundation Symposium","volume":"291 ","pages":"141-54; discussion 154-9, 221-4"},"PeriodicalIF":0.0000,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/9780470754030.ch11","citationCount":"3","resultStr":"{\"title\":\"Cell stress proteins as modulators of bacteria--host interactions.\",\"authors\":\"Brian Henderson\",\"doi\":\"10.1002/9780470754030.ch11\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Multicellular organisms exist in dynamic equilibrium with bacterial populations, either in the form of the microbiota of the organism or as pathogens. A challenge to 21st century systems biology is to determine the networks of interactions that exist between the prokaryotic and eukaryotic components of multicellular organisms. Bacterial colonization is stressful for both the prokaryotic and eukaryotic components of an organism and it is emerging that the cell stress proteins (CSPs) of both bacteria and host play roles in the interaction between both Kingdoms. In addition to acting intracellularly to fold proteins, it is being established that CSPs have a wide range of moonlighting functions that are relevant to controlling bacterial colonization. Thus host CSPs can act as cell surface receptors to bind bacteria or to respond to their components. Host CSPs are also secreted into the extracellular fluid where they modulate leukocyte function, potentially to activate antibacterial defences. Bacteria, in turn, have evolved CSPs with adhesive properties for the host. Bacterial CSPs can also modulate host leukocyte function and can induce cellular apoptosis. In insects, endosymbiotic bacteria provide bacterial CSPs which are utilised by the host. Bacterial CSPs have also been shown to be antibacterial targets. These findings establish a range of roles for CSPs in bacteria-host interactions.</p>\",\"PeriodicalId\":19323,\"journal\":{\"name\":\"Novartis Foundation Symposium\",\"volume\":\"291 \",\"pages\":\"141-54; discussion 154-9, 221-4\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2008-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1002/9780470754030.ch11\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Novartis Foundation Symposium\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1002/9780470754030.ch11\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Novartis Foundation Symposium","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/9780470754030.ch11","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Cell stress proteins as modulators of bacteria--host interactions.
Multicellular organisms exist in dynamic equilibrium with bacterial populations, either in the form of the microbiota of the organism or as pathogens. A challenge to 21st century systems biology is to determine the networks of interactions that exist between the prokaryotic and eukaryotic components of multicellular organisms. Bacterial colonization is stressful for both the prokaryotic and eukaryotic components of an organism and it is emerging that the cell stress proteins (CSPs) of both bacteria and host play roles in the interaction between both Kingdoms. In addition to acting intracellularly to fold proteins, it is being established that CSPs have a wide range of moonlighting functions that are relevant to controlling bacterial colonization. Thus host CSPs can act as cell surface receptors to bind bacteria or to respond to their components. Host CSPs are also secreted into the extracellular fluid where they modulate leukocyte function, potentially to activate antibacterial defences. Bacteria, in turn, have evolved CSPs with adhesive properties for the host. Bacterial CSPs can also modulate host leukocyte function and can induce cellular apoptosis. In insects, endosymbiotic bacteria provide bacterial CSPs which are utilised by the host. Bacterial CSPs have also been shown to be antibacterial targets. These findings establish a range of roles for CSPs in bacteria-host interactions.