Inhibiting platelets aggregation could aggravate the acute infection caused by Staphylococcus aureus.
Several fibrinogen binding proteins (Fibs) play important roles in the pathogenesis of Staphylococcus aureus (S. aureus). Most Fibs can promote the aggregation of platelets during infection, but the extracellular fibrinogen-binding protein (Efb) is an exception. It is reported that Efb can specifically bind fibrinogen and inhibit the aggregation of platelet with its N terminal. However, the biological significance of platelet aggregation inhibition in the infection caused by S. aureus is unclear until now. Here, we demonstrated that the persistence and aggregation of platelets were important for killing S. aureus in whole blood. It was found that the N terminal of Efb (EfbN) and platelets inhibitors could increase the survival of S. aureus in whole blood. The study in vivo also showed that EfbN and platelets inhibitors could reduce the killing of S. aureus and increase the lethality rate of S. aureus in the acute infection mouse model.
Beijing Institute of Basic Medical Sciences, Beijing, P. R. China.
Xin
X
Zhang
Yu
Y
Liu
Yaping
Y
Gao
Jie
J
Dong
Chunhua
C
Mu
Qiang
Q
Lu
Ningsheng
N
Shao
Guang
G
Yang
D000208:Acute Disease; D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D001770:Blood Bactericidal Activity; D001792:Blood Platelets / Q000378:metabolism* / Q000382:microbiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010974:Platelet Aggregation / Q000502:physiology*; D013203:Staphylococcal Infections / Q000097:blood* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000235:genetics / Q000378:metabolism*
D001426:Bacterial Proteins; C114014:Efb protein, Staphylococcus aureus