Assessment of placental cells permissivity to the apicomplexan parasite Toxoplasma gondii from an immunological facet

Abstract

Toxoplasma gondii (T. gondii) is an obligate intracellular parasite capable of infecting humans. T. gondii is the etiologic agent of toxoplasmosis, a disease that is usually asymptomatic to mild symptomatic in immunocompetent individuals, but severe to life threatening in immunocompromised patients. Another spectrum of the disease is the congenital toxoplasmosis whereby the outcome of the disease is highly dependent on the trimester of infection. In primo-infected pregnant women, the first trimester bears the greatest risk of abortion whereas the second and third trimesters bear severe and disabling disease in the developing fetus. T. gondii is known for its ability to hijack macrophages to travel out to various tissues. It also has a great capacity to stimulate and modulate the host immune response. In the current study, we aim at comparing permissivity to T. gondii among placental cell lines and investigating the immune response triggered by the parasite upon infection. In our study, we used three placental cell lines HTR-8, BeWo and JAR, as well as the human macrophages derived from the monocytic THP-1 cell line. All cell lines were infected with the most virulent T. gondii strain (RH HX strain) in a ratio 1 parasite to 10 cells (1:10). The parasite replication was assessed by measuring the transcript levels of the tachyzoite surface marker SAG-1 (Surface Antigen-1). Different pro-inflammatory and anti-inflammatory cytokines transcript levels were also assessed using the Syber green Real time quantitative PCR. Our results show that T. gondii replication capacity in the used placental cells is different from its replication rate in the macrophages, with a higher resistance to the parasite infection in the placental cell lines. This difference in the replication capacity is tightly modulated by a difference in the pro-inflammatory-anti-inflammatory cytokine induced response in the different infected cell systems. As a matter of fact, in almost all tested pro-anti-inflammatory cytokines, a modulation of expressi