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Activation of Plasminogen by Staphylokinase Reduces the Severity of Staphylococcus aureusSystemic Systemic Infection
Sahlgrenska Academy.
Sahlgrenska Academy.
Trinity College, Dublin.
Trinity College, Dublin.
Show others and affiliations
2010 (English)In: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 202, no 7, 1041-1049 p.Article in journal (Refereed) Published
Abstract [en]

 

Background. Theoretical and experimental data support the geographic differentiation strategy as a valuable tool for detecting loci under selection. In the context of Plasmodium falciparum malaria, few populations have been studied, with limited genomic coverage.

Methods. Wild-type S. aureus strain LS-1, which lacks the ability to produce SAK, was modified by an insertion of the sak gene into its chromosome. The sak gene was integrated in 2 forms—(1) linked to its own promoter and (2) fused to the promoter of the protein A gene—which resulted in the overexpression of SAK. SAK is highly specific for human plg and exhibits almost no activity toward murine plg. To investigate the role played by SAK in a murine infection model, human plg transgenic mice and their wild-type counterparts were inoculated intravenously with congenic S. aureus strains differing in SAK production.

Results. Human plg transgenic mice inoculated with SAK-expressing strains displayed significantly reduced mortality, less weight loss, and lower bacterial loads in kidneys than did the wild-type mice. No difference in the severity of sepsis was observed between transgenic and wild-type mice infected with a SAK-deficient strain.

Conclusions. The results suggest that expression of SAK followed by activation of plg alleviates the course of S. aureus sepsis. 

 

 

 

 

 

 

 

 

 

  

 

 

 

 

 

 

 

 

 

 

 

 

 

Background.

 

Staphylokinase (SAK) is produced by the majority of Staphylococcus aureus strains. It is an extracellular protein that activates the conversion of human plasminogen (plg) to plasmin. The role played by SAK in staphylococcal infection is unclear.Methods. Wild-type S. aureus strain LS-1, which lacks the ability to produce SAK, was modified by an insertion of the sak gene into its chromosome. The sak gene was integrated in 2 forms—(1) linked to its own promoter and (2) fused to the promoter of the protein A gene—which resulted in the overexpression of SAK. SAK is highly specific for human plg and exhibits almost no activity toward murine plg. To investigate the role played by SAK in a murine infection model, human plg transgenic mice and their wild-type counterparts were inoculated intravenously with congenic S. aureus strains differing in SAK production.Results. Human plg transgenic mice inoculated with SAK-expressing strains displayed significantly reduced mortality, less weight loss, and lower bacterial loads in kidneys than did the wild-type mice. No difference in the severity of sepsis was observed between transgenic and wild-type mice infected with a SAK-deficient strain.Conclusions. The results suggest that expression of SAK followed by activation of plg alleviates the course of S. aureus

sepsis.

Place, publisher, year, edition, pages
Oxford University Press , 2010. Vol. 202, no 7, 1041-1049 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-64346DOI: 10.1086/656140OAI: oai:DiVA.org:liu-64346DiVA: diva2:389615
Available from: 2011-01-19 Created: 2011-01-19 Last updated: 2017-12-11

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Magnusson, Mattias

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