Mechanisms of Mitochondria-Mediated Apoptosis During Infection.

Coccidiosis in chickens is a parasitic disease caused by species, resulting in significant economic losses to the poultry industry. Among these species, is considered the most virulent pathogen, with its infection strongly associated with the apoptotic response of host cells. modulates host cell apoptosis in a stage-specific manner, suppressing apoptosis in the early phase to promote its intracellular development and triggering apoptosis in later stages to facilitate parasite egress and disease progression. This study established an in vitro infection model using 60 fifteen-day-old chick embryo cecal epithelial cells and infecting the cells with sporozoites at a 1:1 ratio of host cells to sporozoites. The aim was to examine the relationship between parasitic infection and the apoptotic response of host cells in the chick embryo cecal epithelial cells infected with . The roles of the mitochondrial permeability transition pore (MPTP) and cytochrome c in intrinsic apoptosis were examined through the application of cyclosporine A (CsA), N, N, N', N'-tetramethyl-1,4-phenylenediamine (TMPD), and ascorbate (Asc). TUNEL staining, ELISA, and flow cytometry were performed to evaluate apoptotic rates. CsA, TMPD, and Asc significantly ( < 0.01) decreased cytochrome c release, caspase-9 activation, and apoptotic rates from 24 to 120 h post- infection. These findings highlight the significance of cytochrome c-mediated, mitochondria-dependent apoptotic pathways in parasitized chick embryo cecal epithelial cells.