Modulation of ERK and AKT pathways as the potential therapeutic targets for Toxoplasma gondii infection

Toxoplasmosis is a zoonotic disease caused by Toxoplasma gondii, which can infect humans through oocysts or undercooked meat. It can cause varying symptoms, including congenital toxoplasmosis. Early detection and treatment are beneficial, and antimicrobial treatment can prevent or resolve symptoms. The disease has a complex life cycle, with felids being the definitive host. Understanding the signaling pathways is crucial for effective therapeutic strategies. Toxoplasma invasion is regulated by the microtubule cytoskeleton, affecting macrophages and innate immunity cells. Calcium binding proteins and focal adhesion kinase-2 have been identified as key regulators of calcium signaling in Toxoplasma. Calcium signaling is crucial for parasite biology and drug development. The ERK pathway plays a significant role in host-parasite interactions and immune responses. This pathway plays a critical role in the spread of Toxoplasma by manipulating host cell migration. Toxoplasma infection can activate the ERK signaling pathway, leading to the inhibition of apoptosis in host cells. This inhibition of apoptosis is believed to have a positive effect on the survival and replication of the parasite in the host. The Akt signaling pathway, also known as the PI3K/Akt pathway, is crucial in parasitic diseases, modulating host immune responses and parasite survival. Host AKT activation is important for T. gondii proliferation which is related to reduction of ROS in host cells. More investigation is required to fully understand how these signals contribute to the pathophysiology of Toxoplasma infection and to identify possible therapeutic targets for the management of parasitic illnesses.