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Autophagy is a crucial and physiological process for cell survival from yeast to mammals, including protozoan parasites.  Toxoplasma gondii , an intracellular parasite, typically exploits autophagic machinery of host cell; however host cell upregulates autophagy to combat the infection. Herein we tested the efficacy of Rottlerin, a natural polyphenol with autophagic promoting properties, against  Toxoplasma  infection on the chorioncarcinoma-derived cell line BeWo. We found that Rottlerin, at sub-toxic doses, induced morphological and biochemical alterations associated with autophagy and decreased  Toxoplasma  growth in infected cells. Although autophagy was synergically promoted by  Toxoplasma  infection in combination with Rottlerin treatment, the use of the autophagy inhibitor chloroquine revealed that Rottlerin anti-parasitic effect was largely autophagy-independent and likely mediated by the converging inhibitory effect of Rottlerin and  Toxoplasma  in host protein translation, mediated by mTOR inhibition and eIF2α phosphorylation. Both events, which on one hand could explain the additive effect on autophagy induction, on the other hand led to inhibition of protein synthesis, thereby depriving  Toxoplasma  of metabolically essential components for multiplication. We suggest that modulation of the competition between pathogen requirement and host cell defense might be an attractive, novel therapeutic approach against  Toxoplasma  infection and encourage the development of Rottlerin-based new therapeutic formulations.

Rottlerin-mediated inhibition of Toxoplasma gondii growth in BeWo trophoblast-like cells