Complement deposition

Although not the core of this work, it is important to mention biomaterial surface susceptibility to humoral immune complement proteins. According to theory, nucleophilic surfaces, exposing –NH2 (amino groups) or –OH (hydroxyl groups), but not negatively charged surfaces bind complement factor 3b (C3b). C3b in turn binds factors Bb and P forming an active alternative convertase C3bBbP, that subsequently cleaves C3 in solution to C3a and C3b [33]. An amplification mechanism is thereby formed. The surface binding of C3b was recently shown to also be mediated by pre-adsorbed proteins [34]. In yet another study, it was shown that negatively charged surfaces, such as silica and spontaneously oxidized titanium facilitate C3b deposition [35], leading to the hypothesis that complement binds to denatured proteins on surfaces regardless of surface charge. The alternative complement activation pathway is considered to be of greatest importance, and especially in blood contacting applications where a large area of the biomaterial is in contact with blood, such as cardiopulmonary bypass and dialysis apparatus [33].