This study investigated the role of PI3K/Akt signaling pathway on host cell apoptosis in the early infection of Eimeria tenella. Chicken cecal epithelial cells were treated with apoptosis-inducer Actinomycin D (Act D) or PI3K/Akt signaling pathway inhibitor LY294002 and then infected with E. tenella. Results demonstrated that the E. tenella-infected group had less apoptosis 4–8 h after the infection and more apoptosis 12–20 h after the infection than the control group. At 4–20 h after the infection, the apoptotic/necrotic rate and the Caspase-3 activity in the Act D + E. tenella group were lower (P < 0.01) than those in the Act D-treated group. The p-Akt and NF-κB contents in the E. tenella-infected group were higher (P < 0.01) than those in the control group 4–12 h after the infection. However, the bad content and the Caspase-9/3 activity were lower (P < 0.05) in the E. tenella-infected group than in the control group. Compared with the E. tenella-infected group, the LY294002 + E. tenella group showed decreased p-Akt content and increased apoptotic/necrotic rate, bad content, NF-κB expression, membrane permeability transition pore (MPTP) openness, and Caspase-9/3 activity. Thus, the early development of E. tenella could inhibit host cell apoptosis by downregulating the Caspase-3 activity. Upregulating this activity promoted apoptosis. In addition, activating the PI3K/Akt signaling pathway inhibited the apoptosis of E. tenella host cells in the early infection by reducing the expression of the bad content, limiting the MPTP opening, and decreasing the Caspase-9 and Caspase-3 activities.

本研究探讨了PI3K / Akt信号通路在艾美球虫早期感染中对宿主细胞凋亡的作用。用凋亡诱导剂放线菌素D（Act D）或PI3K / Akt信号通路抑制剂LY294002处理鸡盲肠上皮细胞，然后感染大肠杆菌。结果表明，与对照组相比，大肠杆菌感染组在感染后4–8 h凋亡较少，在感染后12–20 h凋亡更多。感染后4–20 h，Act D + E. tenella组的凋亡/坏死率和Caspase-3活性 低于 Act D治疗组（P <0.01）。大肠杆菌中p-Akt和NF-κB的含量感染 后4-12h，感染组高于对照组（P <0.01）。然而，大肠杆菌感染组的不良含量和Caspase-9 / 3活性均低于对照组（P  <0.05）。与大肠杆菌感染的组相比，LY294002 +大肠杆菌感染组的 p-Akt含量降低，细胞凋亡/坏死率，坏菌含量，NF-κB表达，膜通透性转化孔（MPTP）开放性和Caspase- 9/3活动。因此，大肠杆菌的早期发展可能通过下调Caspase-3活性来抑制宿主细胞凋亡。上调这种活性促进细胞凋亡。此外，激活PI3K / Akt信号通路可通过减少有害成分的表达，限制MPTP的开放并降低Caspase-9和Caspase-3的活性来抑制早期感染中的大肠杆菌的宿主细胞的凋亡。