F. Lundberg et al., VITRONECTIN-BINDING STAPHYLOCOCCI ENHANCE SURFACE-ASSOCIATED COMPLEMENT ACTIVATION, Infection and immunity, 65(3), 1997, pp. 897-902
Coagulase-negative staphylococci are well recognized in medical device
-associated infections, Complement activation is known to occur at the
biomaterial surface, resulting in unspecific inflammation around the
biomaterial, The human serum protein vitronectin (Vn), a potent inhibi
tor of complement activation by formation of an inactive terminal comp
lement complex, adsorbs to biomaterial surfaces in contact with blood,
In this report, we discuss the possibility that surface-immobilized V
n inhibits complement activation and the effect of Vn-binding staphylo
cocci on complement activation on surfaces precoated with Vn, The exte
nt of complement activation was measured with a rabbit anti-human C3c
antibody and a mouse anti-human C9 antibody, raised against the neoepi
tope of C9, Our data show that Vn immobilized on a biomaterial surface
retains its ability to inhibit complement activation, The additive co
mplement activation-inhibitory effect of Vn on a heparinized surface i
s very small, In the presence of Vn-binding strain, Staphylococcus hem
olyticus SM131, complement activation on a surface precoated with Vn o
ccurred as it did in the absence of Vn precoating, For S. epidermidis
3380, which does not express binding of Vn, complement activation on a
Vn-precoated surface was significantly decreased, The results could b
e repeated on heparinized surfaces. These data suggest that Vn adsorbe
d to a biomaterial surface may serve to protect against surface-associ
ated complement activation, Furthermore, Vn-binding staphylococcal cel
ls may enhance surface-associated complement activation by blocking th
e inhibitory effect of preadsorbed Vn.