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Abstract

One of virulence factors produced by Staphylococcus aureus is staphylokinase (SAK), which enhances their proteolytic activity leading to tissue damage and improving bacterial invasiveness. In the present study we estimated the ability to produce staphylokinase by 95 S. aureus reference strains and clinical isolates from the airways of cystic fibrosis patients, from skin lesions and from infected bones. We would like to verify any relationship between SAK production and the types of clinical isolates as well as other biochemical properties and activities of these staphylococcal strains, which can be important for their pathogenicity. More than 62% of all tested strains were able to produce secreted type of SAK. Staphylokinase production was significantly more common in the isolates from skin and soft tissue infections than in any other group of tested staphylococci. The general tendencies in the selected properties or activities of both SAK(-) and SAK(+) isolates were similar. Our data confirm phenotypic dissimilarity in SAK production of S. aureus strains isolated from various types of infections. It is compatible with the biological role of staphylokinase and with hypothetical model of staphylokinase mediated bacterial invasion of host tissues. Thus, the estimation of SAK production by S. aureus isolates may be regarded as the parameter describing potential invasiveness of staphylococci and can be useful as a medical recommendation for the eradication of staphylococci carrier state.

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... The sak gene is associated with tissue invasion. 16,17 Its absence could be the reason why most CC15 isolates are associated with carriage rather than invasive infection. ...
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Here we report the draft genome sequence of a bloodstream isolate of methicillin-resistant Staphylococcus aureus strain SA16. Strain SA16 is a sequence type 5 (ST5)-staphylococcal cassette chromosome mec type II (SCCmec II) clone and was the most prevalent isolate at a Brazilian hospital during the second half of 2009.
... The presence of Hla in the filtrates was confirmed by Western blot, using rabbit monoclonal antibody against Hla (Sigma, Germany) diluted 1:5000 in PBS and swine polyclonal antibody against rabbit IgG HRP-conjugated (Dako, Denmark) diluted 1:1,000 in the same buffer. SAK activity was determined by measuring specific plasmin substrate hydrolysis in the presence of 1 lM plasminogen in Tris/ HCl buffer (0.14 M NaCl, 1.5 M Tris-HCl, pH 7.2), as described earlier (Więckowska-Szakiel et al. 2007). ...
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Recently we described a novel bacteriophage-encoded pathogenicity island in Staphylococcus aureus that harbors a number of virulence factors that are all involved in the evasion of innate immunity. Here we describe a mechanism by which staphylokinase (SAK), frequently present on this pathogenicity island, interferes with innate immune defenses: SAK is anti-opsonic. By activating human plasminogen (PLG) into plasmin (PL) at the bacterial surface, it creates bacterium-bound serine protease activity that leads to degradation of two major opsonins: human immunoglobulin G (IgG) and human C3b. Incubation of opsonized bacteria with PLG and SAK resulted in removal of anti-staphylococcal IgGs and C3b from the bacterial surface. In phagocytosis assays this proved to be a very efficient mechanism to reduce the opsonic activity of human IgG and serum. The fact that SAK activates human PLG at the bacterial surface and removes IgG as well as C3b makes this protein a unique anti-opsonic molecule.
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We describe a comprehensive detection system for 18 kinds of classical and newly described staphylococcal superantigenic toxin genes using four sets of multiplex PCR. Superantigenic toxin genotyping of Staphylococcus aureus for 69 food poisoning isolates and 97 healthy human nasal swab isolates revealed 32 superantigenic toxin genotypes and showed that many S. aureus isolates harbored multiple toxin genes. Analysis of the relationship between toxin genotypes and toxin genes encoding profiles of mobile genetic elements suggests its possible role in determining superantigenic toxin genotypes in S. aureus as combinations of toxin gene-encoding mobile genetic elements.
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Staphylococcus aureus can cause superficial skin infections and, occasionally, deep-seated infections that entail spread through the blood stream. The organism expresses several factors that compromise the effectiveness of neutrophils and macrophages, the first line of defence against infection. S. aureus secretes proteins that inhibit complement activation and neutrophil chemotaxis or that lyse neutrophils, neutralizes antimicrobial defensin peptides, and its cell surface is modified to reduce their effectiveness. The organism can survive in phagosomes, express polysaccharides and proteins that inhibit opsonization by antibody and complement, and its cell wall is resistant to lysozyme. Furthermore, S. aureus expresses several types of superantigen that corrupt the normal humoral immune response, resulting in anergy and immunosuppression. In contrast, Staphylococcus epidermidis must rely primarily on cell-surface polymers and the ability to form a biolfilm to survive in the host.