SalK/SalR, a two-component signal transduction system, is essential for full virulence of highly invasive Streptococcus suis serotype 2
Streptococcus suis serotype 2 (S. suis 2, SS2) has evolved into a highly infectious entity, which caused the two recent large-scale outbreaks of human SS2 epidemic in China, and is characterized by a toxic shock-like syndrome. However, the molecular pathogenesis of this new emerging pathogen is stil...
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| Veröffentlicht in: | PloS one 2008-05, Vol.3 (5), p.e2080 |
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| creator | Li, Ming Wang, Changjun Feng, Youjun Pan, Xiuzhen Cheng, Gong Wang, Jing Ge, Junchao Zheng, Feng Cao, Min Dong, Yaqing Liu, Di Wang, Jufang Lin, Ying Du, Hongli Gao, George F Wang, Xiaoning Hu, Fuquan Tang, Jiaqi |
| description | Streptococcus suis serotype 2 (S. suis 2, SS2) has evolved into a highly infectious entity, which caused the two recent large-scale outbreaks of human SS2 epidemic in China, and is characterized by a toxic shock-like syndrome. However, the molecular pathogenesis of this new emerging pathogen is still poorly understood.
89K is a newly predicted pathogenicity island (PAI) which is specific to Chinese epidemic strains isolated from these two SS2 outbreaks. Further bioinformatics analysis revealed a unique two-component signal transduction system (TCSTS) located in the candidate 89K PAI, which is orthologous to the SalK/SalR regulatory system of Streptococcus salivarius. Knockout of salKR eliminated the lethality of SS2 in experimental infection of piglets. Functional complementation of salKR into the isogenic mutant DeltasalKR restored its soaring pathogenicity. Colonization experiments showed that the DeltasalKR mutant could not colonize any susceptible tissue of piglets when administered alone. Bactericidal assays demonstrated that resistance of the mutant to polymorphonuclear leukocyte (PMN)-mediated killing was greatly decreased. Expression microarray analysis exhibited a transcription profile alteration of 26 various genes down-regulated in the DeltasalKR mutant.
These findings suggest that SalK/SalR is requisite for the full virulence of ethnic Chinese isolates of highly pathogenic SS2, thus providing experimental evidence for the validity of this bioinformatically predicted PAI. |
| doi_str_mv | 10.1371/journal.pone.0002080 |
| format | Article |
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89K is a newly predicted pathogenicity island (PAI) which is specific to Chinese epidemic strains isolated from these two SS2 outbreaks. Further bioinformatics analysis revealed a unique two-component signal transduction system (TCSTS) located in the candidate 89K PAI, which is orthologous to the SalK/SalR regulatory system of Streptococcus salivarius. Knockout of salKR eliminated the lethality of SS2 in experimental infection of piglets. Functional complementation of salKR into the isogenic mutant DeltasalKR restored its soaring pathogenicity. Colonization experiments showed that the DeltasalKR mutant could not colonize any susceptible tissue of piglets when administered alone. Bactericidal assays demonstrated that resistance of the mutant to polymorphonuclear leukocyte (PMN)-mediated killing was greatly decreased. Expression microarray analysis exhibited a transcription profile alteration of 26 various genes down-regulated in the DeltasalKR mutant.
These findings suggest that SalK/SalR is requisite for the full virulence of ethnic Chinese isolates of highly pathogenic SS2, thus providing experimental evidence for the validity of this bioinformatically predicted PAI.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0002080</identifier><identifier>PMID: 18461172</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Apoptosis ; Bacterial Proteins - genetics ; Bacterial Proteins - physiology ; Bioengineering ; Bioinformatics ; Biotechnology ; Cellular signal transduction ; Cloning ; Colonization ; Complementation ; DNA microarrays ; E coli ; Epidemics ; Epidemiology ; Escherichia coli ; Experimental infection ; Gene Deletion ; Gene expression ; Genomes ; Granulocytes ; Immunology ; Infectious Diseases/Bacterial Infections ; Kinases ; Laboratories ; Lethality ; Leukocytes (polymorphonuclear) ; Medicine ; Meningitis ; Microbiology ; Microbiology/Cellular Microbiology and Pathogenesis ; Microbiology/Immunity to Infections ; Microbiology/Medical Microbiology ; Neutrophils ; Outbreaks ; Pathogenesis ; Pathogenicity ; Pathogens ; Polyamide-imides ; Promoter Regions, Genetic ; Septic shock ; Serotyping ; Signal Transduction ; Streptococcal Infections - transmission ; Streptococcal Infections - veterinary ; Streptococcus ; Streptococcus infections ; Streptococcus pneumoniae ; Streptococcus suis - classification ; Streptococcus suis - genetics ; Streptococcus suis - pathogenicity ; Swine ; Swine Diseases - microbiology ; Swine Diseases - transmission ; Transcription ; Transcription (Genetics) ; Transcription, Genetic ; Transduction ; Vectors (Biology) ; Virulence ; Virulence Factors - genetics</subject><ispartof>PloS one, 2008-05, Vol.3 (5), p.e2080</ispartof><rights>COPYRIGHT 2008 Public Library of Science</rights><rights>2008 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Li et al. 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c728t-fcf53d58e9c07413d0560da06d0a09130cd5926ee2ccf13590d2a23d6ec4783f3</citedby><cites>FETCH-LOGICAL-c728t-fcf53d58e9c07413d0560da06d0a09130cd5926ee2ccf13590d2a23d6ec4783f3</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/PMC2358977/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2358977/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18461172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Beier, Dagmar</contributor><creatorcontrib>Li, Ming</creatorcontrib><creatorcontrib>Wang, Changjun</creatorcontrib><creatorcontrib>Feng, Youjun</creatorcontrib><creatorcontrib>Pan, Xiuzhen</creatorcontrib><creatorcontrib>Cheng, Gong</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Ge, Junchao</creatorcontrib><creatorcontrib>Zheng, Feng</creatorcontrib><creatorcontrib>Cao, Min</creatorcontrib><creatorcontrib>Dong, Yaqing</creatorcontrib><creatorcontrib>Liu, Di</creatorcontrib><creatorcontrib>Wang, Jufang</creatorcontrib><creatorcontrib>Lin, Ying</creatorcontrib><creatorcontrib>Du, Hongli</creatorcontrib><creatorcontrib>Gao, George F</creatorcontrib><creatorcontrib>Wang, Xiaoning</creatorcontrib><creatorcontrib>Hu, Fuquan</creatorcontrib><creatorcontrib>Tang, Jiaqi</creatorcontrib><title>SalK/SalR, a two-component signal transduction system, is essential for full virulence of highly invasive Streptococcus suis serotype 2</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Streptococcus suis serotype 2 (S. suis 2, SS2) has evolved into a highly infectious entity, which caused the two recent large-scale outbreaks of human SS2 epidemic in China, and is characterized by a toxic shock-like syndrome. However, the molecular pathogenesis of this new emerging pathogen is still poorly understood.
89K is a newly predicted pathogenicity island (PAI) which is specific to Chinese epidemic strains isolated from these two SS2 outbreaks. Further bioinformatics analysis revealed a unique two-component signal transduction system (TCSTS) located in the candidate 89K PAI, which is orthologous to the SalK/SalR regulatory system of Streptococcus salivarius. Knockout of salKR eliminated the lethality of SS2 in experimental infection of piglets. Functional complementation of salKR into the isogenic mutant DeltasalKR restored its soaring pathogenicity. Colonization experiments showed that the DeltasalKR mutant could not colonize any susceptible tissue of piglets when administered alone. Bactericidal assays demonstrated that resistance of the mutant to polymorphonuclear leukocyte (PMN)-mediated killing was greatly decreased. Expression microarray analysis exhibited a transcription profile alteration of 26 various genes down-regulated in the DeltasalKR mutant.
These findings suggest that SalK/SalR is requisite for the full virulence of ethnic Chinese isolates of highly pathogenic SS2, thus providing experimental evidence for the validity of this bioinformatically predicted PAI.</description><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Bacterial Proteins - genetics</subject><subject>Bacterial Proteins - physiology</subject><subject>Bioengineering</subject><subject>Bioinformatics</subject><subject>Biotechnology</subject><subject>Cellular signal transduction</subject><subject>Cloning</subject><subject>Colonization</subject><subject>Complementation</subject><subject>DNA microarrays</subject><subject>E coli</subject><subject>Epidemics</subject><subject>Epidemiology</subject><subject>Escherichia coli</subject><subject>Experimental infection</subject><subject>Gene Deletion</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Granulocytes</subject><subject>Immunology</subject><subject>Infectious Diseases/Bacterial Infections</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Lethality</subject><subject>Leukocytes (polymorphonuclear)</subject><subject>Medicine</subject><subject>Meningitis</subject><subject>Microbiology</subject><subject>Microbiology/Cellular Microbiology and Pathogenesis</subject><subject>Microbiology/Immunity to Infections</subject><subject>Microbiology/Medical Microbiology</subject><subject>Neutrophils</subject><subject>Outbreaks</subject><subject>Pathogenesis</subject><subject>Pathogenicity</subject><subject>Pathogens</subject><subject>Polyamide-imides</subject><subject>Promoter Regions, Genetic</subject><subject>Septic shock</subject><subject>Serotyping</subject><subject>Signal Transduction</subject><subject>Streptococcal Infections - transmission</subject><subject>Streptococcal Infections - veterinary</subject><subject>Streptococcus</subject><subject>Streptococcus infections</subject><subject>Streptococcus pneumoniae</subject><subject>Streptococcus suis - classification</subject><subject>Streptococcus suis - genetics</subject><subject>Streptococcus suis - pathogenicity</subject><subject>Swine</subject><subject>Swine Diseases - microbiology</subject><subject>Swine Diseases - transmission</subject><subject>Transcription</subject><subject>Transcription (Genetics)</subject><subject>Transcription, Genetic</subject><subject>Transduction</subject><subject>Vectors (Biology)</subject><subject>Virulence</subject><subject>Virulence Factors - genetics</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2LEzEUhgdR3HX1H4gGBEHYdvMxk8ncCMviR3FhYavehjRzMs2STrpJptpf4N82taO2F4IEkpA85z0nJ29RPCd4SlhNLu78EHrlpmvfwxRjTLHAD4pT0jA64RSzhwf7k-JJjHcYV0xw_rg4IaLkhNT0tPgxV-7TRZ5uz5FC6ZufaL_aSfYJRdvlBCgF1cd20Mn6HsVtTLA6RzYiiDFTNhPGB2QG59DGhsFBrwF5g5a2W7otsv1GRbsBNE8B1slrr_UQURyyRITg03YNiD4tHhnlIjwb17Piy_t3n68-Tq5vPsyuLq8nuqYiTYw2FWsrAY3GdUlYiyuOW4V5ixVuCMO6rRrKAajWhrCqwS1VlLUcdFkLZthZ8XKvu3Y-yrGHURJGKBU1J2UmZnui9epOroNdqbCVXln568CHTqqQrHYgtRGlAKUbVi5KsTALEI2pcAugCWe8zlpvx2zDYgWtzv0Kyh2JHt_0dik7v5GUVaKpdwKvRoHg7weI6R8lT_dUp3JVtjc-i-k8WlhZnT_T2Hx-WdaUV5TRKge8OQrITILvqVNDjHI2v_1_9ubrMfv6gF2CcmkZvRt21onHYLkHdfAxBjB_ekKw3Nn79zvlzotytHcOe3HYz79Bo5_ZT5ze-O4</recordid><startdate>20080507</startdate><enddate>20080507</enddate><creator>Li, Ming</creator><creator>Wang, Changjun</creator><creator>Feng, Youjun</creator><creator>Pan, Xiuzhen</creator><creator>Cheng, Gong</creator><creator>Wang, Jing</creator><creator>Ge, Junchao</creator><creator>Zheng, Feng</creator><creator>Cao, Min</creator><creator>Dong, Yaqing</creator><creator>Liu, Di</creator><creator>Wang, Jufang</creator><creator>Lin, Ying</creator><creator>Du, Hongli</creator><creator>Gao, George F</creator><creator>Wang, Xiaoning</creator><creator>Hu, Fuquan</creator><creator>Tang, Jiaqi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20080507</creationdate><title>SalK/SalR, a two-component signal transduction system, is essential for full virulence of highly invasive Streptococcus suis serotype 2</title><author>Li, Ming ; Wang, Changjun ; Feng, Youjun ; Pan, Xiuzhen ; Cheng, Gong ; Wang, Jing ; Ge, Junchao ; Zheng, Feng ; Cao, Min ; Dong, Yaqing ; Liu, Di ; Wang, Jufang ; Lin, Ying ; Du, Hongli ; Gao, George F ; Wang, Xiaoning ; Hu, Fuquan ; Tang, Jiaqi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c728t-fcf53d58e9c07413d0560da06d0a09130cd5926ee2ccf13590d2a23d6ec4783f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Bacterial Proteins - 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transmission</topic><topic>Streptococcal Infections - veterinary</topic><topic>Streptococcus</topic><topic>Streptococcus infections</topic><topic>Streptococcus pneumoniae</topic><topic>Streptococcus suis - classification</topic><topic>Streptococcus suis - genetics</topic><topic>Streptococcus suis - pathogenicity</topic><topic>Swine</topic><topic>Swine Diseases - microbiology</topic><topic>Swine Diseases - transmission</topic><topic>Transcription</topic><topic>Transcription (Genetics)</topic><topic>Transcription, Genetic</topic><topic>Transduction</topic><topic>Vectors (Biology)</topic><topic>Virulence</topic><topic>Virulence Factors - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Ming</creatorcontrib><creatorcontrib>Wang, Changjun</creatorcontrib><creatorcontrib>Feng, Youjun</creatorcontrib><creatorcontrib>Pan, Xiuzhen</creatorcontrib><creatorcontrib>Cheng, Gong</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Ge, Junchao</creatorcontrib><creatorcontrib>Zheng, Feng</creatorcontrib><creatorcontrib>Cao, Min</creatorcontrib><creatorcontrib>Dong, Yaqing</creatorcontrib><creatorcontrib>Liu, Di</creatorcontrib><creatorcontrib>Wang, Jufang</creatorcontrib><creatorcontrib>Lin, Ying</creatorcontrib><creatorcontrib>Du, Hongli</creatorcontrib><creatorcontrib>Gao, George F</creatorcontrib><creatorcontrib>Wang, Xiaoning</creatorcontrib><creatorcontrib>Hu, Fuquan</creatorcontrib><creatorcontrib>Tang, Jiaqi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Ming</au><au>Wang, Changjun</au><au>Feng, Youjun</au><au>Pan, Xiuzhen</au><au>Cheng, Gong</au><au>Wang, Jing</au><au>Ge, Junchao</au><au>Zheng, Feng</au><au>Cao, Min</au><au>Dong, Yaqing</au><au>Liu, Di</au><au>Wang, Jufang</au><au>Lin, Ying</au><au>Du, Hongli</au><au>Gao, George F</au><au>Wang, Xiaoning</au><au>Hu, Fuquan</au><au>Tang, Jiaqi</au><au>Beier, Dagmar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SalK/SalR, a two-component signal transduction system, is essential for full virulence of highly invasive Streptococcus suis serotype 2</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2008-05-07</date><risdate>2008</risdate><volume>3</volume><issue>5</issue><spage>e2080</spage><pages>e2080-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Streptococcus suis serotype 2 (S. suis 2, SS2) has evolved into a highly infectious entity, which caused the two recent large-scale outbreaks of human SS2 epidemic in China, and is characterized by a toxic shock-like syndrome. However, the molecular pathogenesis of this new emerging pathogen is still poorly understood.
89K is a newly predicted pathogenicity island (PAI) which is specific to Chinese epidemic strains isolated from these two SS2 outbreaks. Further bioinformatics analysis revealed a unique two-component signal transduction system (TCSTS) located in the candidate 89K PAI, which is orthologous to the SalK/SalR regulatory system of Streptococcus salivarius. Knockout of salKR eliminated the lethality of SS2 in experimental infection of piglets. Functional complementation of salKR into the isogenic mutant DeltasalKR restored its soaring pathogenicity. Colonization experiments showed that the DeltasalKR mutant could not colonize any susceptible tissue of piglets when administered alone. Bactericidal assays demonstrated that resistance of the mutant to polymorphonuclear leukocyte (PMN)-mediated killing was greatly decreased. Expression microarray analysis exhibited a transcription profile alteration of 26 various genes down-regulated in the DeltasalKR mutant.
These findings suggest that SalK/SalR is requisite for the full virulence of ethnic Chinese isolates of highly pathogenic SS2, thus providing experimental evidence for the validity of this bioinformatically predicted PAI.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>18461172</pmid><doi>10.1371/journal.pone.0002080</doi><tpages>e2080</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2008-05, Vol.3 (5), p.e2080 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1312287614 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Analysis Animals Apoptosis Bacterial Proteins - genetics Bacterial Proteins - physiology Bioengineering Bioinformatics Biotechnology Cellular signal transduction Cloning Colonization Complementation DNA microarrays E coli Epidemics Epidemiology Escherichia coli Experimental infection Gene Deletion Gene expression Genomes Granulocytes Immunology Infectious Diseases/Bacterial Infections Kinases Laboratories Lethality Leukocytes (polymorphonuclear) Medicine Meningitis Microbiology Microbiology/Cellular Microbiology and Pathogenesis Microbiology/Immunity to Infections Microbiology/Medical Microbiology Neutrophils Outbreaks Pathogenesis Pathogenicity Pathogens Polyamide-imides Promoter Regions, Genetic Septic shock Serotyping Signal Transduction Streptococcal Infections - transmission Streptococcal Infections - veterinary Streptococcus Streptococcus infections Streptococcus pneumoniae Streptococcus suis - classification Streptococcus suis - genetics Streptococcus suis - pathogenicity Swine Swine Diseases - microbiology Swine Diseases - transmission Transcription Transcription (Genetics) Transcription, Genetic Transduction Vectors (Biology) Virulence Virulence Factors - genetics |
| title | SalK/SalR, a two-component signal transduction system, is essential for full virulence of highly invasive Streptococcus suis serotype 2 |
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