Inflammatory pathways of Toxoplasma gondii infection in pregnancy

Abstract

Toxoplasma gondii (T. gondii), an obligate intracellular parasite, is considered as an opportunistic infection and causes toxoplasmosis in humans and animals. Congenital toxoplasmosis can influence pregnancy and cause mild to severe consequences for the fetal and neonatal. During early T. gondii infection, neutrophils as the most abundant white blood cells provide a front line of defense mechanism against infection. The activated dendritic cells are then responsible for initiating an inflammatory response via T-helper 1 (Th1) cells. As part of its robust immune response, the infected host cells produce interferon (IFN-γ). IFN-γ inhibits T. gondii replication and promotes its transformation from an active form to tissue cysts. Although anti- T. gondii antibodies play an important role in infection control, T-helper 2 (Th2) immune response, can facilitate the growth and proliferation of T. gondii in the host cell. In pregnant women infected with T. gondii, the expression of cytokines may vary and in response diverse outcomes are expected. Cytokine profiles serve as valuable indicators for estimating the patho-immunological effects of T. gondii infection. This demonstrates the intricate relationship between pro-inflammatory and anti-inflammatory cytokines, as well as their influence on the various pregnancy outcomes in T. gondii infection.