Calcium homeostasis in mitochondrion-mediated apoptosis of chick embryo cecal epithelial cells induced by Eimeria tenella infection

- We examined the role of Ca2 + in mitochondrial apoptosis during Eimeria tenella infection.
- Cytosolic [Ca2 +] and apoptosis increased in chick cecal epithelial cells infected by Eimeria tenella.
- The increases were abolished by blocking extracellular Ca2 + influx and ER Ca2 + channel release.
- Restoring Ca2 + homeostasis can suppress apoptosis induced by Eimeria tenella infection.

In this study, the process of Eimeria tenella-induced apoptosis and the effect of calcium homeostasis were investigated in chick embryo cecal epithelial cells. In particular, we examined cytochrome c release into the cytoplasm, mitochondrial permeability transition pore (MPTP) opening, and changes in [Ca2 +]c and apoptosis in host cells. Apoptosis, MPTP opening, cytochrome c release, and [Ca2 +]c in host cells increased following infection. This trend was reversed by blocking the increase in [Ca2 +]c using BAPTA/AM and EGTA (intra- and extracellular chelators of Ca2 +, respectively) and by applying heparin sodium and ryanodine (blockers of the inositol triphosphate and ryanodine receptors of the endoplasmic reticulum, respectively). These results indicate that [Ca2 +]c plays a significant role in host cell mitochondrial apoptosis, which is induced via modulation of extracellular Ca2 + levels and endoplasmic reticulum Ca2 + channels. Thus, agents that restore Ca2 + homeostasis may be useful for managing E. tenella infection in chickens.