Staphylococcus aureus Fur Regulates the Expression of Virulence Factors That Contribute to the Pathogenesis of Pneumonia
The tremendous success of Staphylococcus aureus as a pathogen is due to the controlled expression of a diverse array of virulence factors. The effects of host environments on the expression of virulence factors and the mechanisms by which S. aureus adapts to colonize distinct host tissues are largel...
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| Veröffentlicht in: | Infection and Immunity 2010-04, Vol.78 (4), p.1618-1628 |
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| creator | Torres, Victor J Attia, Ahmed S Mason, William J Hood, M. Indriati Corbin, Brian D Beasley, Federico C Anderson, Kelsi L Stauff, Devin L McDonald, W. Hayes Zimmerman, Lisa J Friedman, David B Heinrichs, David E Dunman, Paul M Skaar, Eric P |
| description | The tremendous success of Staphylococcus aureus as a pathogen is due to the controlled expression of a diverse array of virulence factors. The effects of host environments on the expression of virulence factors and the mechanisms by which S. aureus adapts to colonize distinct host tissues are largely unknown. Vertebrates have evolved to sequester nutrient iron from invading bacteria, and iron availability is a signal that alerts pathogenic microorganisms when they enter the hostile host environment. Consistent with this, we report here that S. aureus senses alterations in the iron status via the ferric uptake regulator (Fur) and alters the abundance of a large number of virulence factors. These Fur-mediated changes protect S. aureus against killing by neutrophils, and Fur is required for full staphylococcal virulence in a murine model of infection. A potential mechanistic explanation for the impact of Fur on virulence is provided by the observation that Fur coordinates the reciprocal expression of cytolysins and a subset of immunomodulatory proteins. More specifically, S. aureus lacking fur exhibits decreased expression of immunomodulatory proteins and increased expression of cytolysins. These findings reveal that Fur is involved in initiating a regulatory program that organizes the expression of virulence factors during the pathogenesis of S. aureus pneumonia. |
| doi_str_mv | 10.1128/IAI.01423-09 |
| format | Article |
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Indriati ; Corbin, Brian D ; Beasley, Federico C ; Anderson, Kelsi L ; Stauff, Devin L ; McDonald, W. Hayes ; Zimmerman, Lisa J ; Friedman, David B ; Heinrichs, David E ; Dunman, Paul M ; Skaar, Eric P</creator><creatorcontrib>Torres, Victor J ; Attia, Ahmed S ; Mason, William J ; Hood, M. Indriati ; Corbin, Brian D ; Beasley, Federico C ; Anderson, Kelsi L ; Stauff, Devin L ; McDonald, W. Hayes ; Zimmerman, Lisa J ; Friedman, David B ; Heinrichs, David E ; Dunman, Paul M ; Skaar, Eric P</creatorcontrib><description>The tremendous success of Staphylococcus aureus as a pathogen is due to the controlled expression of a diverse array of virulence factors. The effects of host environments on the expression of virulence factors and the mechanisms by which S. aureus adapts to colonize distinct host tissues are largely unknown. Vertebrates have evolved to sequester nutrient iron from invading bacteria, and iron availability is a signal that alerts pathogenic microorganisms when they enter the hostile host environment. Consistent with this, we report here that S. aureus senses alterations in the iron status via the ferric uptake regulator (Fur) and alters the abundance of a large number of virulence factors. These Fur-mediated changes protect S. aureus against killing by neutrophils, and Fur is required for full staphylococcal virulence in a murine model of infection. A potential mechanistic explanation for the impact of Fur on virulence is provided by the observation that Fur coordinates the reciprocal expression of cytolysins and a subset of immunomodulatory proteins. More specifically, S. aureus lacking fur exhibits decreased expression of immunomodulatory proteins and increased expression of cytolysins. These findings reveal that Fur is involved in initiating a regulatory program that organizes the expression of virulence factors during the pathogenesis of S. aureus pneumonia.</description><identifier>ISSN: 0019-9567</identifier><identifier>EISSN: 1098-5522</identifier><identifier>DOI: 10.1128/IAI.01423-09</identifier><identifier>PMID: 20100857</identifier><identifier>CODEN: INFIBR</identifier><language>eng</language><publisher>Washington, DC: American Society for Microbiology</publisher><subject>Animals ; Bacterial Proteins - biosynthesis ; Bacterial Proteins - genetics ; Bacterial Proteins - physiology ; Bacteriology ; Biological and medical sciences ; Chromatography, Liquid ; Disease Models, Animal ; Electrophoresis, Gel, Two-Dimensional ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; Gene Knockout Techniques ; Mass Spectrometry ; Mice ; Mice, Inbred C57BL ; Microbiology ; Miscellaneous ; Molecular Genomics ; Pneumonia, Staphylococcal - microbiology ; Proteome - analysis ; Repressor Proteins - genetics ; Repressor Proteins - physiology ; Staphylococcus aureus - pathogenicity ; Staphylococcus aureus - physiology ; Virulence Factors - biosynthesis</subject><ispartof>Infection and Immunity, 2010-04, Vol.78 (4), p.1618-1628</ispartof><rights>2015 INIST-CNRS</rights><rights>Copyright © 2010, American Society for Microbiology 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c506t-9c9a386d4798237ba73804c01092f2bc89b6aec5f9bc714e92336794a6d8076c3</citedby><cites>FETCH-LOGICAL-c506t-9c9a386d4798237ba73804c01092f2bc89b6aec5f9bc714e92336794a6d8076c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849423/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849423/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,3188,3189,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22556167$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20100857$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Torres, Victor J</creatorcontrib><creatorcontrib>Attia, Ahmed S</creatorcontrib><creatorcontrib>Mason, William J</creatorcontrib><creatorcontrib>Hood, M. 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Indriati</au><au>Corbin, Brian D</au><au>Beasley, Federico C</au><au>Anderson, Kelsi L</au><au>Stauff, Devin L</au><au>McDonald, W. Hayes</au><au>Zimmerman, Lisa J</au><au>Friedman, David B</au><au>Heinrichs, David E</au><au>Dunman, Paul M</au><au>Skaar, Eric P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Staphylococcus aureus Fur Regulates the Expression of Virulence Factors That Contribute to the Pathogenesis of Pneumonia</atitle><jtitle>Infection and Immunity</jtitle><addtitle>Infect Immun</addtitle><date>2010-04-01</date><risdate>2010</risdate><volume>78</volume><issue>4</issue><spage>1618</spage><epage>1628</epage><pages>1618-1628</pages><issn>0019-9567</issn><eissn>1098-5522</eissn><coden>INFIBR</coden><abstract>The tremendous success of Staphylococcus aureus as a pathogen is due to the controlled expression of a diverse array of virulence factors. The effects of host environments on the expression of virulence factors and the mechanisms by which S. aureus adapts to colonize distinct host tissues are largely unknown. Vertebrates have evolved to sequester nutrient iron from invading bacteria, and iron availability is a signal that alerts pathogenic microorganisms when they enter the hostile host environment. Consistent with this, we report here that S. aureus senses alterations in the iron status via the ferric uptake regulator (Fur) and alters the abundance of a large number of virulence factors. These Fur-mediated changes protect S. aureus against killing by neutrophils, and Fur is required for full staphylococcal virulence in a murine model of infection. A potential mechanistic explanation for the impact of Fur on virulence is provided by the observation that Fur coordinates the reciprocal expression of cytolysins and a subset of immunomodulatory proteins. More specifically, S. aureus lacking fur exhibits decreased expression of immunomodulatory proteins and increased expression of cytolysins. These findings reveal that Fur is involved in initiating a regulatory program that organizes the expression of virulence factors during the pathogenesis of S. aureus pneumonia.</abstract><cop>Washington, DC</cop><pub>American Society for Microbiology</pub><pmid>20100857</pmid><doi>10.1128/IAI.01423-09</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Bacterial Proteins - biosynthesis Bacterial Proteins - genetics Bacterial Proteins - physiology Bacteriology Biological and medical sciences Chromatography, Liquid Disease Models, Animal Electrophoresis, Gel, Two-Dimensional Female Fundamental and applied biological sciences. Psychology Gene Expression Profiling Gene Expression Regulation, Bacterial Gene Knockout Techniques Mass Spectrometry Mice Mice, Inbred C57BL Microbiology Miscellaneous Molecular Genomics Pneumonia, Staphylococcal - microbiology Proteome - analysis Repressor Proteins - genetics Repressor Proteins - physiology Staphylococcus aureus - pathogenicity Staphylococcus aureus - physiology Virulence Factors - biosynthesis |
| title | Staphylococcus aureus Fur Regulates the Expression of Virulence Factors That Contribute to the Pathogenesis of Pneumonia |
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