Protein FOG - a streptococcal inhibitor of neutrophil function

Surface proteins of group G Streptococcus in different phases of growth: patterns of production and implications for the host–bacteria relationship

“…At this point the two surface proteins were cleaved from the bacterial surface with trypsin. PG binds HSA, whereas FOG has affinity for fibrinogen (Johansson et al, 2004;Sjöbring et al, 1988), and binding experiments with 125 I-labelled HSA and fibrinogen confirmed that trypsin efficiently removes FOG and PG from the surface of G45 bacteria. Following trypsin digestion, the bacteria were resuspended in their stationary-phase growth medium and the samples were then incubated at 37 u C to continue the stationary phase.…”

“…PG and FOG bind HSA and fibrinogen, respectively, with high affinity and specificity (Johansson et al, 2004;Sjöbring et al, 1988). To visualize PG and FOG at the surface, bacteria from different growth phases were incubated with gold-labelled HSA (5 nm colloidal gold) and fibrinogen (10 nm colloidal gold), and subjected to negative staining and EM.…”

“…Like bradykinin, these two peptides induce an increased vascular permeability. In addition, FOG binds fibrinogen to form complexes, which, analogously to the M protein of group A streptococci (Herwald et al, 2004), activate neutrophils to release heparin-binding protein (Johansson et al, 2004), another pro-inflammatory substance inducing vascular leakage of plasma. Since plasma is rich in nutrients, these multiple permeability-increasing effects of FOG should increase the nutrients available for bacterial growth.…”

“…These cover the bacterial surface and interact with several host proteins and defence systems. For example, PG and the M-like protein FOG bind several human plasma proteins (Björck & Kronvall, 1984;Björck et al, 1987;Johansson et al, 2004;Nitsche-Schmitz et al, 2007;Reis et al, 1984;Wollein Waldetoft et al, 2012), including components of the complement and contact systems, but the effects they exert are different; FOG activates these systems whereas PG protects the bacteria against the antibacterial peptides generated through the activation Wollein Waldetoft et al, 2012).…”

“…The suspension was distributed into tubes with 10 ml in each, and incubated at 37 uC with 5 % CO 2 for 26 h with or without 0.2 mg ml 21 chloramphenicol, or kept cold (4 uC) for the same period. Following incubation, the bacteria were subjected to binding assays with 125 I-labelled human serum albumin (HSA; Sigma) or fibrinogen (Sigma), which bind PG and FOG, respectively (Johansson et al, 2004;Sjöbring et al, 1988), as described in Wollein Waldetoft et al (2012). The experiment was performed in 12 replicates in three blocks.…”