It is probably due to the reason that when E. granulosus invaded, the hydatid cyst established is potentially able to activate host complement [32], resulting in the upregulation of C3a release, which attract and active inflammatory cells, thereby releasing the proinflammation cytokines, as suggested by the upregulation of CXCL2 che-mokines. It has been known that various complement cleavage products have effector functions. C3 ligate their seven transmembrane-spanning G protein-coupled receptors C3aR, transmitting proinflammatory signals that induce vasodilation and cytokine and chemokine release [30].