The surface charge of trypanosomatids of the genus trypanosoma

Souto-Padrón, Thaïs; Chiari, Égler; Souza, Wanderley de

doi:10.1590/s0074-02761990000200013

Cited by 5 publications

(4 citation statements)

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“…Although we were yet to determine which kind of endocytosis was responsible for the uptake of the cationic bacteriocin AS-48, it was tempting to think that it could take place once it had interacted with anionic residues on the outer surface of the parasite ( Souto-Padrón et al, 1990 ), as suggested for the neuropeptide VIP, another cationic trypanocidal peptide believed to bind to negatively charged glycoproteins such as VSG ( Gonzalez-Rey et al, 2006 ).…”

Section: Resultsmentioning

confidence: 99%

Autophagic-related cell death of Trypanosoma brucei induced by bacteriocin AS-48

Martínez‐García

Bart

Campos‐Salinas

et al. 2018

International Journal for Parasitology: Drugs and Drug Resistan

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The parasitic protozoan Trypanosoma brucei is the causative agent of human African trypanosomiasis (sleeping sickness) and nagana. Current drug therapies have limited efficacy, high toxicity and/or are continually hampered by the appearance of resistance. Antimicrobial peptides have recently attracted attention as potential parasiticidal compounds. Here, we explore circular bacteriocin AS-48's ability to kill clinically relevant bloodstream forms of T. brucei gambiense, T. brucei rhodesiense and T. brucei brucei. AS-48 exhibited excellent anti-trypanosomal activity in vitro (EC50 = 1–3 nM) against the three T. brucei subspecies, but it was innocuous to human cells at 104-fold higher concentrations. In contrast to its antibacterial action, AS-48 does not kill the parasite through plasma membrane permeabilization but by targeting intracellular compartments. This was evidenced by the fact that vital dye internalization-prohibiting concentrations of AS-48 could kill the parasite at 37 °C but not at 4 °C. Furthermore, AS-48 interacted with the surface of the parasite, at least in part via VSG, its uptake was temperature-dependent and clathrin-depleted cells were less permissive to the action of AS-48. The bacteriocin also caused the appearance of myelin-like structures and double-membrane autophagic vacuoles. These changes in the parasite's ultrastructure were confirmed by fluorescence microscopy as AS-48 induced the production of EGFP-ATG8.2-labeled autophagosomes. Collectively, these results indicate AS-48 kills the parasite through a mechanism involving clathrin-mediated endocytosis of VSG-bound AS-48 and the induction of autophagic-like cell death. As AS-48 has greater in vitro activity than the drugs currently used to treat T. brucei infection and does not present any signs of toxicity in mammalian cells, it could be an attractive lead compound for the treatment of sleeping sickness and nagana.

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Section: Resultsmentioning

confidence: 99%

Autophagic-related cell death of Trypanosoma brucei induced by bacteriocin AS-48

Martínez‐García

Bart

Campos‐Salinas

et al. 2018

International Journal for Parasitology: Drugs and Drug Resistan

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“…The presence of these two subpopulations suggests the presence of distinct evolutive forms in the same sample. It is important to notice that transitional forms, characterized by the presence of a rod-shaped kinetoplast located at the nuclear side and which display some surface characteristics of trypomastigotes, such as the same mean electrophoretic mobility (Souto-Padrón et al 1990a), are frequently found free in the culture medium in variable amounts even when Dm28c parasites are maintained in LIT medium. No data are known about the behavior of transitional forms which incubated in the presence of lectins.…”

Section: Pna-binding Sitesmentioning

confidence: 99%

“…In the case of parasites obtained from axenic media, it has been shown that growth conditions interfere with cell surface composition, as evaluated in studies of parasite-host cell interaction (Araújo-Jorge 1989) and cell agglutination using lectins (Pereira et al 1980;Andrade et al 1991), although they do not interfere with the cell surface charge (Souto-Padrón et al 1984, 1990aDe Souza 1985, 1986).…”

Section: Introductionmentioning

confidence: 99%

Localization of lectin-binding sites on the surface of Trypanosoma cruzi grown in chemically defined conditions

Bourguignon

Souza²,

Souto-Padrón³

1998

Histochemistry and Cell Biology

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The transformation of Trypanosoma cruzi epimastigotes to mammal-infective metacyclic trypomastigotes (metacyclogenesis) can be performed in vitro under chemically defined conditions (TAU 3AAG medium). During this process, changes in the nature of cell surface sugar composition and sugar distribution was evaluated using FITC and gold-labeled lectins and observed by flow cytometry and transmission electron microscopy. The pattern of labeling with the lectins from Triticum vulgaris (WGA), Arachis hypogaea (PNA), Limax flavus (LFA), Canavalia ensiformis (Con-A), and Ricinus communis (RCA-I) significantly changed during the metacyclogenic process. The results obtained are discussed in relation to the role played by T. cruzi cell surface carbohydrate residues on the process of parasite-host cell interaction.

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“…Uma notável característica do T. cruzi é sua heterogeneidade biológica e bioquímica. Os parasitas apresentam diferenças notáveis no seu crescimento, tropismo tissular, composição antigênica e virulência, bem como uma diferente susceptibilidade à quimioterapia e na sua resistência a alguns dos mecanismos da resposta imune (ALCANTARA;BRENER, 1978;SOUTO-PADRON et al, 1990;MARTINEZ-DIAZ;ESARIO et al;2001;CORTEZ et al, 2006).…”

Section: O Parasita E Os Modelos Murinos De Infecçãounclassified

Dinâmica das células T reguladoras (TREG) na infecção murina pelo Trypanosoma cruzi e o seu eventual envolvimento na patologia cardíaca na fase crônica.

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The surface charge of trypanosomatids of the genus trypanosoma

Cited by 5 publications

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Autophagic-related cell death of Trypanosoma brucei induced by bacteriocin AS-48

Autophagic-related cell death of Trypanosoma brucei induced by bacteriocin AS-48

Localization of lectin-binding sites on the surface of Trypanosoma cruzi grown in chemically defined conditions

Dinâmica das células T reguladoras (TREG) na infecção murina pelo Trypanosoma cruzi e o seu eventual envolvimento na patologia cardíaca na fase crônica.

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