Synthetic immunostimulatory glycans interference with host cell apoptosis upon of Toxoplasma gondii infection, in vitro


Toxoplasmosis is a protozoan infection of humans and animals caused by Toxoplasma gondii, and it’s continuous public health and food safety issue. The tachyzoites (Tg) of T. gondii are the most important stage, as they come in direct contact with immune cells such as a macrophage. Tg can modulate and prevent apoptosis of immune cells while promoting survival of the pathogen. Infections caused by Tg can be eradicated if immune cells could stimulate apoptosis and kill pathogens upon exposure. Apoptosis is characterized by the release of mediators, namely Caspases (Cas). New means are required for inducing apoptosis and enhance immunity in the infected host cell to control toxoplasmosis. The present study investigated whether Synthetic Immuno-stimulatory Glycans (SIGs) influence Cas and Nitric oxide (NO) release and led to Tg damage. Galβ1-3Gal-PAA-fluor (SIG1), Fucα1-4GlcNAcβ-PAA-fluor (SIG2) and GlcNAcβ1-3GalNAcα-PAA-fluor (SIG3) constituted samples studied principally. Murine macrophage had been exposed to the Tg then the SIGs effects on Cas and NO production were determined after 20 hours of pathogen phagocytosis. Here we report that the SIGs had potent in vitro activity against T. gondii; SIG2 was more effective than SIG1 and SIG3, representative by SIG2 treated infected macrophages can induced infected macrophages to release Cas1, 3, and 9. Maximum production of NO by infected macrophages was noticed following the expoxure to all SIGs. Therefore the present study provided the method for the selection of SIGs ligands bearing immunostimulatory factor and apoptotic stimuli properties.