2006
DOI: 10.1096/fj.06-5804fje
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Trigger for group A streptococcal M1T1 invasive disease

Abstract: The globally disseminated Streptococcus pyogenes M1T1 clone causes a number of highly invasive human diseases. The transition from local to systemic infection occurs by an unknown mechanism; however invasive M1T1 clinical isolates are known to express significantly less cysteine protease SpeB than M1T1 isolates from local infections. Here, we show that in comparison to the M1T1 strain 5448, the isogenic mutant ∆speB accumulated 75-fold more human plasmin activity on the bacterial surface following incubation i… Show more

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Cited by 139 publications
(168 citation statements)
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“…These observations suggest that, for PAM-positive S. pyogenes strains, the specific interaction between human plasminogen kringle 2 domain, subcluster 2b streptokinase and plasminogen binding M proteins provides selection pressure for the co-inheritance of these GAS virulence factors (8,11). A number of PAM-negative GAS strains, including GAS serotype M1T1, also demonstrate human plasminogen dependent virulence (7,26,40) We therefore hypothesise that PAMpositive and PAM-negative GAS strains employ differing strategies for surface plasminogen acquisition and activation. For PAM-negative isolates, the formation of a trimolecular complex of streptokinase, plasminogen and fibrinogen, bound to the GAS cell surface via fibrinogen receptors or the plasminogen receptors α-enolase and GAPDH may represent an alternative human plasminogen-dependent virulence pathway employed by this strain set (11,13,34,41).…”
Section: Discussionmentioning
confidence: 93%
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“…These observations suggest that, for PAM-positive S. pyogenes strains, the specific interaction between human plasminogen kringle 2 domain, subcluster 2b streptokinase and plasminogen binding M proteins provides selection pressure for the co-inheritance of these GAS virulence factors (8,11). A number of PAM-negative GAS strains, including GAS serotype M1T1, also demonstrate human plasminogen dependent virulence (7,26,40) We therefore hypothesise that PAMpositive and PAM-negative GAS strains employ differing strategies for surface plasminogen acquisition and activation. For PAM-negative isolates, the formation of a trimolecular complex of streptokinase, plasminogen and fibrinogen, bound to the GAS cell surface via fibrinogen receptors or the plasminogen receptors α-enolase and GAPDH may represent an alternative human plasminogen-dependent virulence pathway employed by this strain set (11,13,34,41).…”
Section: Discussionmentioning
confidence: 93%
“…Mutanolysin extracts and GAS culture supernatants from overnight cultures were prepared as described previously (26). Following SDS-PAGE of the protein samples according to the method of Laemmli (27), proteins were transferred to nitrocellulose membrane using a Bio-Rad Trans-Blot apparatus (Bio-Rad, USA).…”
Section: Determination Of M Protein Streptokinase Gapdh and -Enolamentioning
confidence: 99%
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“…This natural resistance of mice to severe GAS sepsis can be overcome by the use of high infectious doses, less resistant strains or transgenic mice carrying human HLA class II 18 or human plasminogen. 45,46 Despite this, successful attempts were made with standard inbred mouse lines, for example, BALB/c, C3H/HeN and CBA/J, C57BL/10 17 and DBA/2 and C57BL/6 (Kansal and Kotb, personal communication); whereas these studies were quite informative, conventional mouse models are limited in their genetic pool, and thus one may miss important genotype-trait relations. Our choice was thus to use one of the genetically diversified mouse reference populations generated by the international Complex Trait Consortium (CTC).…”
Section: Discussionmentioning
confidence: 99%