Initial inflammatory and haemostatic mechanisms induced by endogenous and bioartificial surfaces in a whole blood model

Inflammation is a hallmark of atherosclerosis, and an important factor determining biomedical devices biocompatibility. We hypothesis both events could involve surface activation phenomenon’s. Cholesterol crystals (CC) represent an endogenous surface formed upon crystallization of cholesterol and associated to atherosclerotic plaques. Microcapsules for pancreatic beta cells transplantation in diabetes treatment suffers from bioincompatibility problems. We postulate the inflammatory phenomenon’s could involve the same endogenous activators. Of the earliest endogenous activators are the complement and coagulation proteins, which are increasingly recognized as contributors in inflammation and disease. The systems are connected through several interacting points as illustrated. Presently we are studying cross-talk mechanisms within these systems in a whole blood model. Briefly, our data indicates that Cholesterol crystals activate both complement and coagulation factors, with complement as the initial trigger. For alginate microcapsules the activation sequence is dependent on the capsules compositions. While poly-L-lysine containing microcapsules activates firstly the complement and secondly the coagulation system, the cellulose-sulfate containing microcapsules are potent and early coagulation activators. Last, we have shown that inflammatory cytokine secretion can be solely dependent on complement activation, a phenomenon probably linked to the integrin CD11b and cell-adhesion.