Effect of ATP and Bax on the apoptosis of Eimeria tenella host cells

• Main Authors: Zhiyong Xu, Mingxue Zheng, Li Zhang, Xuesong Zhang, Yan Zhang, Xiaozhen Cui, Xin Gong, Rou Xi, Rui Bai
• Format: Article
• Language: English
• Published: BMC 2017-12-01
• Series: BMC Veterinary Research
• Subjects: Eimeria tenella; Host cell; Apoptosis; ATP; Bax
• Online Access: http://link.springer.com/article/10.1186/s12917-017-1313-z

Abstract Background Eimeria tenella (E. tenella) is a species of Eimeria that causes haemorrhagic caecal coccidiosis, resulting in major economic losses in the global poultry industry. After E. tenella infection, the amount of ATP and Bax in host cells showed highly significant changes. Therefore, it is necessary to investigate the effects of ATP and Bax on the apoptosis of E. tenella host cells. Results The ATP-treated group and the V5-treated group had higher E. tenella infection rates than the untreated group at 24, 48, 72, 96, and 120 h after infection with E. tenella. The results of flow cytometry showed that compared with the control group, the mitochondrial permeability transition pore (MPTP) opening in the untreated group was highly significantly increased (P < 0.01) at 4, 24, 48, 72, 96, and 120 h. Moreover, results from Hoechst-Annexin V-PI staining and flow cytometry showed that the rates of early apoptosis, late apoptosis, and necrosis in the untreated group were significantly lower (P < 0.05) or highly significantly lower (P < 0.01) than those of the control group at 4 h, while the rates of early apoptosis, late apoptosis, and necrosis in the untreated group were higher at varying degrees than those in the control group at 24–120 h (P < 0.05 or P < 0.01). After treatment with ATP and Bax inhibitors, the rates of early apoptosis, late apoptosis, and necrosis, in addition to the MPTP opening in both the ATP-treated and V5-treated groups, were significantly lower (P < 0.05) or highly significantly lower (P < 0.01) than those in the untreated group. Conclusions ATP and Bax play important roles in regulating the apoptosis of E. tenella host cells.