Eimeria tenellamainly invades and develops into cecal epithelial cells of chickens, resulting in cecal epithelial cell damage. Infectious intracellular pathogens possibly act by influencing the autophagy process after invading cells. The interaction between E. tenellaand the autophagy of host cells was explored by infecting E. tenellawith chick embryo cecal epithelial cells. Transmission electron microscopy, laser confocal microscopy, and Western blot analysis were used to demonstrate that E. tenellainfection could induce autophagy in host cells. Results showed that infection with E. tenellainduced the formation of autophagosomes in cells. The expression of ATG 5, Beclin-1, and LC3B-II proteins were significantly (P< 0.01) increased after E. tenellainfected host cells. Expression of p62 protein levels were significantly (P< 0.01) decreased in host cells infected with E. tenella. Chloroquine (CQ) significantly (P< 0.01) increased the expression levels of LC3B-II and P62 in E. tenella-infected host cells. Rapamycin (RAPA) induced autophagy in host cells, thus reducing the intracellular infection of E. tenella. By contrast, the infection rate of E. tenellaincreased in cells treated with 3-Methyladenine (3-MA). Hence, E. tenellasporozoite infection could induce autophagy activation in chick embryo cecal epithelial cells, and enhanced autophagy could reduce the infection rate of E. tenella.