title: SalK/SalR, a two-component signal transduction system, is essential for full virulence of highly invasive Streptococcus suis serotype 2.
abstract: BACKGROUND
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Microbiology, Third Military Medical University, Chongqing, China.
authors.forename: Ming
authors.initials: M
authors.lastname: Li
authors.forename: Changjun
authors.initials: C
authors.lastname: Wang
authors.forename: Youjun
authors.initials: Y
authors.lastname: Feng
authors.forename: Xiuzhen
authors.initials: X
authors.lastname: Pan
authors.forename: Gong
authors.initials: G
authors.lastname: Cheng
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Junchao
authors.initials: J
authors.lastname: Ge
authors.forename: Feng
authors.initials: F
authors.lastname: Zheng
authors.forename: Min
authors.initials: M
authors.lastname: Cao
authors.forename: Yaqing
authors.initials: Y
authors.lastname: Dong
authors.forename: Di
authors.initials: D
authors.lastname: Liu
authors.forename: Jufang
authors.initials: J
authors.lastname: Wang
authors.forename: Ying
authors.initials: Y
authors.lastname: Lin
authors.forename: Hongli
authors.initials: H
authors.lastname: Du
authors.forename: George F
authors.initials: GF
authors.lastname: Gao
authors.forename: Xiaoning
authors.initials: X
authors.lastname: Wang
authors.forename: Fuquan
authors.initials: F
authors.lastname: Hu
authors.forename: Jiaqi
authors.initials: J
authors.lastname: Tang
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics* / Q000502:physiology; D017353:Gene Deletion; D011401:Promoter Regions, Genetic; D012703:Serotyping; D015398:Signal Transduction; D013290:Streptococcal Infections / Q000635:transmission / Q000662:veterinary*; D017011:Streptococcus suis / Q000145:classification / Q000235:genetics* / Q000472:pathogenicity*; D013552:Swine; D013553:Swine Diseases / Q000382:microbiology* / Q000635:transmission; D014158:Transcription, Genetic; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics*
chemical_list: D001426:Bacterial Proteins; D037521:Virulence Factors