Toxoplasma gondii induces MLTC-1 apoptosis via ERS pathway

Toxoplasma gondii (T. gondii) is an opportunistic parasitic protozoan that can infect the nucleated cells of warm-blooded animals (Abdul Hafeez et al., 2022). Toxoplasmosis is a serious zoonotic disease (Yang et al., 2020; Zhang et al., 2020). The life cycle of T. gondii is complex, with a wide range of intermediate hosts, among which felines are the only final hosts (Almeria and Dubey, 2021; Dubey, 2009; Hill and Dubey, 2002). Toxoplasmosis is mostly a recessive infection with a low incidence rate (Zhao and Ewald, 2020; Mammari et al., 2019). If the disease occurs, toxoplasma infection can cause damage to multiple organ systems. This has a greater impact on females, resulting in miscarriage, stillbirth, or a deformed fetus, in addition to the damage of male reproductive organs, thereby affecting sperm motility and fertility. As such, toxoplasma infections can seriously endanger public health (Harker et al., 2015; Bigna et al., 2020; Ajioka and Morrissette, 2009).

Apoptosis is a gene-regulated process of automatic cell death that helps maintain homeostasis in the internal environment, which is a mechanism used by the body to defend against pathogen infection (Chu et al., 2017). After a pathogen infects a cell, the host initiates an apoptosis program to help the immune system kill the pathogen (Pan et al., 2017). Cryptosporidium parvum, Leishmania, T. gondii, and other intracellular parasites can regulate the apoptosis of host cells to ensure their own survival (Goebel et al., 2001; Carmen et al., 2006; Hippe et al., 2008). Zhou (Zhou et al., 2019) found that Toxoplasma infection could inhibit the apoptosis of glial cells or immune cells. Wang demonstrated that Toxoplasma infection caused endoplasmic reticulum stress. This led to mitochondrial dysfunction and induced human small intestinal epithelial cell apoptosis (Wang et al., 2021a). Wei found that T. gondii granulin 15 induced apoptosis of choriocarcinoma jeg-3 cells through endoplasmic reticulum stress (Wei et al., 2018).

Leydig cells are important reproductive cells in male animals and T. gondii infection can damage these cells. MLTC-1 cells are often used to study the physiological functions of Leydig cells in vitro. We conducted a series of experiments to investigate the effect and mechanism of T. gondii infection on MLTC-1 apoptosis. Flow cytometry showed that T. gondii infection caused significant apoptosis of MLTC-1 cells. RT-qPCR and western blot detected the expression of apoptosis-related proteins and unfolded protein response-related proteins. UPR is a kind of self-protection response. When cells undergo endoplasmic reticulum stress, expression of the UPR protein can reduce the stress conditions. If the damage is too large to attenuate by UPR, cells may mediate apoptosis through the ERS pathway.

留言 (0)

沒有登入
gif