Fig. 5: Tryptophan catabolites decide the fate of T. gondii replication.

a Wild type (Wt), and IDO1-knock-out (KO) cells were incubated with or without tryptophan and T. gondii growth was checked by qPCR (ITS-1), and immunoblot (SAG1), and average ± SE of intensity of band of three similar blots were denoted in bar diagram. *p < 0.01 and ^#p < 0.01, evaluation was made relative to corresponding time-point, infected with only parasite. b Caco2 cells were infected with T. gondii in absence and presence of tryptophan, with or without IFN-γ, and growth of parasite and IDO1 expression were determined by qPCR. Parasite growth (SAG1), IDO1, phopsho-AKT, total AKT and phospho-β-catenin expression were checked by immnoblotting and the average of three repeats were expressed in bar diagram with error bars using β-actin as internal control. *p < 0.05 c Similarly, Wt, IDO1KO, IDO1 restored by HA-IDO1 plasmid in IDO1KO cells were infected with parasite in presence or absence of IFN-γ. ITS-1 expression was determined by qPCR and SAG1 expression was determined by immunoblot. The mean ± SE of three repeats were expressed in bar diagram with error bars using β-actin as internal control. *p < 0.001