An Integrated Model of Biphasic Apoptosis in Avian Coccidiosis: Molecular Networks and Host–Parasite Interplay

Coccidiosis is one of the most serious parasitic diseases in poultry, with <i>Eimeria</i>-induced apoptosis of IECs recognized as a key pathogenic mechanism. This review systematically delineates the molecular mechanisms governing this apoptotic process. The invasion process of <i>Eimeria</i> app. is mediated by the AMA1-RON2 moving junction complex and secreted effector proteins. An integrated model of apoptotic regulation is proposed. This model comprises the mitochondrial, death receptor, and endoplasmic reticulum stress pathways, which are coordinated by signaling hubs, such as PI3K/Akt, NF-κB, and JNK/p38 MAPK, and is further finely modulated by non-coding RNA networks. It is notable that the apoptosis during coccidial infection exhibits a biphasic pattern, where early inhibition supports parasite development and late activation facilitates parasite release and dissemination. Although potential therapeutic targets have emerged for these signaling pathways, how the host precisely switches between different apoptotic pathways remains a current core knowledge gap. Future research needs to thoroughly analyze the molecular logic of host-parasite interaction and ultimately lay a theoretical foundation for developing new strategies targeting the process of cell apoptosis for coccidiosis prevention and control.