Fig. 8

Schematic model of apoptosis by T. vaginalis in SiHa cells. Trichomonas vaginalis induces apoptosis through mitochondrial ROS and ER stress response, and also induces ROS-dependent ER stress response and ER stress-mediated mitochondrial dysfunction through the IRE1/ASK1/JNK/Bcl-2 family protein pathways, finally leading to apoptosis of the SiHa cells. In addition, T. vaginalis ESP also exerted mitochondrial ROS production, apoptosis and ER stress response in SiHa cells. Collectively, T. vaginalis infection induces apoptosis via ROS–ER stress-mitochondrial apoptosis pathways by interaction with mitochondria and ER in human cervical cancer SiHa cells, and this pathogenesis may be involved in the ESP released from live T. vaginalis