In short, from the above phenomenon, we concluded that it may be due to the inflammation effect mediated by complement, as the complement was a key trigger of innate inflammation in E. granulosus infection. At 8wks, the larval stage or metacestode of E. granulosus (hydatid cyst) causes a chronic infection, the complement involved in the immune system was activated, which attract and activate inflammatory cells, thereby releasing the chemoattractants CXCL2, thus initi-ate an early phase of neutrophil recruitment. In the process of fighting against the parasite, these cells release histamine and other biologically active molecular, thereby causing blood vessels to dilate capillaries through increased permeability, smooth muscle contraction, thus mediate local inflammation [30, 32, 34]. Our results are in partial agreements with reports on E. granulosus infection in mice, showing that the hydatid cyst establishment are associated with the control of complement system and, consequently, of local inflammation at the early stages of infection [32].