Figure 1
In vivo lifecycle highlighting the metacyclogenesis process and updated view of in vitro T. cruzi metacyclogenesis. (A) As contextualized in the Introduction, the parasite has two hosts. In its vertebrate host, the infective metacyclic trypomastigote form comes into contact with mammals through wounds or mucosal exposure, and the parasite then changes into its amastigote replicative form. After intense multiplication, it breaks the cells of the vertebrate host, and the blood trypomastigote form is exposed to the bloodstream. Subsequently, the mammal is bitten by the triatomine, and the trypomastigote blood form of the parasite undergoes differentiation into the epimastigote form in the posterior intestine of the invertebrate host. In the rectal surface of the triatomine the epimastigote form adheres and then differentiates in the metacyclic trypomastigote form. (B) For in vitro metacyclogenesis, after three exponential phase passages (3 × 107 parasites/mL), the axenic epimastigotes were allowed to reach the end of the exponential phase (5 × 107 parasites/mL). The epimastigotes were then subjected to nutritional stress in TAU medium (nutritional stress of 2 h) and later differentiated into the metacyclic trypomastigote form (6–96 h of metacyclogenesis). The number of adhered epimastigotes was estimated based on the total number of parasites subjected to metacyclogenesis (5 × 106 parasites/mL) and their relation with the epimastigote and trypomastigote forms throughout the process. The AdhM form was the combination of Ad12 and Ad24h, and Ad48 and Ad72h were denoted AdlM. The data were statistically analysed by two-way analysis of variance (two-way ANOVA) and Tukey’s test for the comparison of averages (mean values ± S.D. from three independent experiments, each of which with technical duplicates). The symbols indicate the following: #not significant, *p < 0.05 and ***p < 0.001.
