Staphylococcus aureus proteins Sbi and Efb recruit human plasmin to degrade complement C3 and C3b.
Staphylococcus aureus proteins Sbi and Efb recruit human plasmin to degrade complement C3 and C3b.
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DOI:
10.1371/journal.pone.0047638
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Skerka C
中科院分区:
文献类型:
--
作者:
Koch TK;Reuter M;Barthel D;Böhm S;van den Elsen J;Kraiczy P;Zipfel PF;Skerka C
Upon host infection, the human pathogenic microbe Staphylococcus aureus (S. aureus) immediately faces innate immune reactions such as the activated complement system. Here, a novel innate immune evasion strategy of S. aureus is described. The staphylococcal proteins surface immunoglobulin-binding protein (Sbi) and extracellular fibrinogen-binding protein (Efb) bind C3/C3b simultaneously with plasminogen. Bound plasminogen is converted by bacterial activator staphylokinase or by host-specific urokinase-type plasminogen activator to plasmin, which in turn leads to degradation of complement C3 and C3b. Efb and to a lesser extend Sbi enhance plasmin cleavage of C3/C3b, an effect which is explained by a conformational change in C3/C3b induced by Sbi and Efb. Furthermore, bound plasmin also degrades C3a, which exerts anaphylatoxic and antimicrobial activities. Thus, S. aureus Sbi and Efb comprise platforms to recruit plasmin(ogen) together with C3 and its activation product C3b for efficient degradation of these complement components in the local microbial environment and to protect S. aureus from host innate immune reactions.
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影响因子:
4.7
作者:
Laarman, Alexander;Milder, Fin;van Strijp, Jos;Rooijakkers, Suzan
通讯作者:
Rooijakkers, Suzan
影响因子:
8
作者:
Haspel, Nurit;Ricklin, Daniel;Lambris, John D.
通讯作者:
Lambris, John D.
DOI:
10.4049/jimmunol.0903678
发表时间:
2010-11-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Amara U;Flierl MA;Rittirsch D;Klos A;Chen H;Acker B;Brückner UB;Nilsson B;Gebhard F;Lambris JD;Huber-Lang M
通讯作者:
Huber-Lang M
DOI:
10.1084/jem.20070818
发表时间:
2007-10-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Jongerius I;Köhl J;Pandey MK;Ruyken M;van Kessel KP;van Strijp JA;Rooijakkers SH
通讯作者:
Rooijakkers SH
影响因子:
6.4
作者:
Lee, LYL;Höök, M;Brown, EL
通讯作者:
Brown, EL