Fig. 3.

Fibrinogen binding hinders GAS clearance by the host innate immune system and enhances GAS virulence. a Resistance to whole blood killing in the absence (Ancrod+) or presence (Ancrod−) of endogenous fibrinogen. b Resistance to neutrophil killing in the absence (minus sign) or presence (plus sign) of exogenous fibrinogen (Fg). c Extracellular killing by neutrophils in which phagocytosis was blocked (cytochalasin D) in the absence (minus sign) or presence (plus sign) of fibrinogen. d NETs formation by neutrophils was induced by addition of PMA before the survival of GAS was examined in the absence (minus sign) or presence (plus sign) of fibrinogen. e, f C57Bl/6 mice were infected subcutaneously with GAS M1 and GAS M1* into the opposite flanks. e Time course of skin lesions size after GAS M1 and GAS M1* infection. f At day 4, the infected skin of the animals shown in (e) was harvested and homogenised to enumerate surviving bacteria. a–d Data were pooled from three independent experiments done in triplicate, mean ± SEM; *p < 0.05; **p < 0.01; ***p < 0.001. e, f Data were pooled from two independent experiments, N = 11; *p < 0.05