| 1. |
- Khil, J, et al.
(författare)
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Plasminogen enhances virulence of group A streptococci by streptokinase-dependent and streptokinase-independent mechanisms
- 2003
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Ingår i: Journal of Infectious Diseases. - : Oxford University Press (OUP). - 1537-6613 .- 0022-1899. ; 188:4, s. 497-505
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Tidskriftsartikel (refereegranskat)abstract
- Interactions between host plasminogen (Plg) and streptokinase (SK) secreted by group A streptococci ( GAS) have been hypothesized to promote bacterial invasion of tissues. The virulence of GAS strain UMAA2616, after being subcutaneously inoculated into mice, was studied. Skin lesions and mortality were observed after inoculation of 7 x 10(6) cfu. Coadministration of human Plg with UMAA2616 markedly increased virulence. SK-deficient UMAA2616 (UMAA2616-SK-) was generated. Mean skin-lesion area and mortality, after bacterial inoculation (3 x 10(5) cfu), were significantly greater with UMAA2616 in the presence of human Plg than with UMAA2616-SK- in the presence of human Plg (P = .0001). Human Plg also enhanced UMAA2616-SK- vir ulence. Exogenous human Plg enhanced the virulence of MGAS166, a human clinical isolate. These findings suggest that SK-Plg interactions are an important determinant of GAS invasiveness in vivo and that both SK and host Plg activators appear to promote virulence of GAS by catalyzing plasmin formation.
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| 2. |
- Sun, HM, et al.
(författare)
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Plasminogen is a critical host pathogenicity factor for group A streptococcal infection
- 2004
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Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 1095-9203 .- 0036-8075. ; 305:5688, s. 1283-1286
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Tidskriftsartikel (refereegranskat)abstract
- Group A streptococci, a common human pathogen, secrete streptokinase, which activates the host's blood clot-dissolving protein, plasminogen. Streptokinase is highly specific for human plasminogen, exhibiting little or no activity against other mammalian species, including mouse. Here, a transgene expressing human plasminogen markedly increased mortality in mice infected with streptococci, and this susceptibility was dependent on bacterial streptokinase expression. Thus, streptokinase is a key pathogenicity factor and the primary determinant of host species specificity for group A streptococcal infection. In addition, local fibrin clot formation may be implicated in host defense against microbial pathogens.
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