Ultrastructural and physiological changes induced by different stress conditions on the human parasite Trypanosoma cruzi

Abstract

Trypanosoma cruzi is the etiological agent of Chagas disease. The life cycle of this protozoan parasite is digenetic because it alternates its different developmental forms through two hosts, a vector insect and a vertebrate host. As a result, the parasites are exposed to sudden and drastic environmental changes causing cellular stress. The stress response to some types of stress has been studied in T. cruzi, mainly at the molecular level; however, data about ultrastructure and physiological state of the cells in stress conditions are scarce or null. In this work, we analyzed the morphological, ultrastructural, and physiological changes produced on T. cruzi epimastigotes when they were exposed to acid, nutritional, heat, and oxidative stress. Clear morphological changes were observed, but the physiological conditions varied depending on the type of stress. The maintenance of the physiological state was severely affected by heat shock, acidic, nutritional, and oxidative stress. According to the surprising observed growth recovery after damage by stress alterations, different adaptations from the parasite to these harsh conditions were suggested. Particular cellular death pathways are discussed.

Stress Induces Release of Extracellular Vesicles by Trypanosoma cruzi Trypomastigotes

“…Under acidic conditions, epimastigotes, the forms found in the vector, release membrane lipids [41]. Trypanosoma cruzi epimastigotes exhibit changes in morphology, especially in epimastigotes [42], which after 24 h induce large metabolic alterations [43]. However, it is still unclear how acidic conditions induce Journal of Immunology Research parasite changes over short periods.…”

A Promising Amphotericin B Derivative Induces Morphological Alterations, Mitochondrial Damage, and Oxidative Stress In Vitro and Prevents Mice from Death Produced by a Virulent Strain of Trypanosoma cruzi

“…Epimastigotes (2 × 10 6 /mL) were incubated with A21 (5 or 10 µM) for 30 and 60 min. Treated parasites were harvested, washed, and resuspended in cold PBS for 45 min in the dark with 10 µM DCFDA at 28 • C. Epimastigotes treated with 160 µM H 2 O 2 were used as a positive control, as reported previously [19]. The oxidation of DCFDA was determined by the fluorescent product 2, 7 dichlorofluorescein (DCF in a Sinergy H1 microplate reader (Biotek, Winooski, VT, USA) (λex of 488 nm and λem of 530 nm).…”

“…Then, alterations in the fluorescence intensities for Rho 123 (FL1-H) were quantified by the Index of Variation (IV) that was obtained using the equation (TM − CM)/CM, where TM is the median of fluorescence for treated parasites and CM is the median of fluorescence for control parasites (untreated). Negative values of IV correspond to the depolarization of the mitochondrial membrane [19].…”

Environmental influence on <em>Triatoma vitticeps</em> occurrence and <em>Trypanosoma cruzi</em> infection in the Atlantic Forest of south-eastern Brazil

“…Contrary to the effect of real-time air humidity, the relationship between temperature and T. cruzi infection has been more thoroughly investigated, especially regarding how ambient temperature can influence T. cruzi infection in triatomines (Asin & Catalá, 1995;Pérez-Morales et al, 2017;de Fuentes-Vicente et al, 2018). Under laboratory conditions, T. cruzi has been shown to develop faster in T. infestans as the temperature increased (Asin and Catalá, 1995), while increased metacyclogenesis with increasing temperature has been observed in R. prolixus specimens (Tamayo et al, 2018).…”