Compared to the co-incubation model which employed addition of CPPs to the donor blood in the flow culture system, intravenous administration of CPPs to Wistar rats induced significantly higher production of monocyte-derived chemokines (MIP-1α, MIP-3α, CINC-1, CINC-3, CXCL10), whilst an upregulation of sICAM-1 and IL-8 suggested a notable contribution of endothelial dysfunction to the CPP-triggered systemic inflammatory response. The gene discussed is CXCL10; the disease is endothelial dysfunction.