Amastigotes
Amastigotes - Related Videos
06:13
Introducing a Gene Knockout Directly Into the Amastigote Stage of Trypanosoma cruzi Using the CRISPR/Cas9 System
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Cited by 5 •
2019
Here, we describe a protocol to introduce a gene knockout into the extracellular amastigote of Trypanosoma cruzi, using the CRISPR/Cas9 system. The growth phenotype can be followed up either by cell counting of axenic amastigote culture or by proliferation of intracellular amastigotes after host cell invasion.
05:55
In Vivo Imaging of Leishmania infantum-infected Hamsters by Gingival Inoculation of Axenic Amastigotes Expressing Luciferase
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2025
Here we present a longitudinal evaluation of golden hamsters infected intraperitoneally (IP) or via intragingival (IG) with L. infantum-Luc by bioluminescent imaging and by PCR. Hamsters were evaluated 1 day post infection (1 dpi), 1 week after infection (8 dpi), and 3 weeks after infection (22 dpi) and euthanized at the 50th dpi and 8 months post infection.
08:17
Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs
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Cited by 3 •
2022
The present protocol describes light-sheet fluorescent microscopy and automated software-assisted methods to visualize and precisely quantify proliferating and dormant Trypanosoma cruzi parasites and T cells in intact, cleared organs and tissues. These techniques provide a reliable way to evaluate treatment outcomes and offer new insights into parasite-host interactions.
12:22
A Parasite Rescue and Transformation Assay for Antileishmanial Screening Against Intracellular Leishmania donovani Amastigotes in THP1 Human Acute Monocytic Leukemia Cell Line
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Cited by 118 •
2012
A parasite-rescue and transformation assay with THP1 cells infected in vitro with Leishmania donovani has been optimized for anti-leishmanial drug screening. The assay involves differentiation of THP1 cells, infection with promastigotes, treatment with test drugs, controlled lysis of the infected macrophages, rescue of amastigotes, transformation to promastigotes and monitoring promastigote growth and proliferation with a fluorometric assay.
03:40
β-Galactosidase Assay to Evaluate Drug-Induced Cytotoxicity in Parasites
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2023
In this video, we describe a simple and robust method to determine the cytotoxic potential of a trypanocidal drug against a parasite, Trypanosoma cruzi, expressing the β-galactosidase enzyme. β-galactosidase serves as a cell lysis indicator, and its activity can be used to assess the effects of the drug.
FAQs
Adaptation follows entry into mammalian host cells, when motile forms differentiate into the intracellular stage and adjust to conditions within either phagolysosomal compartments or the host-cell cytoplasm. This transition links parasite development to the host environment, enabling researchers to examine how cellular location and context support persistence during infection.
Location determines which host-cell environment the parasite must tolerate. Amastigotes may occupy phagolysosomal compartments or the host-cell cytoplasm, providing distinct contexts for studying parasite survival, multiplication, and interaction with cellular defenses. Comparing these locations can help connect intracellular habitat with persistent infection and with differences in tissue damage associated with kinetoplastid diseases.
Binary fission allows amastigotes to increase their numbers while remaining associated with mammalian host cells. This process matters because intracellular multiplication can be examined alongside parasite persistence and host-cell effects, including tissue damage. Observing changes linked to division helps researchers connect a life-cycle process with infection outcomes and the evaluation of antiparasitic strategies.
Amastigotes provide a model for examining how a parasite remains within mammalian cells despite host defenses. Their intracellular persistence allows investigation of host-pathogen interactions and immune evasion, while associated tissue damage supplies a disease-relevant outcome. This focus links cellular behavior to broader infection biology rather than treating parasite development as an isolated life-cycle event.
Researchers can identify amastigotes by considering their distinctive morphology together with their intracellular location. These features support recognition of the relevant life-cycle stage in biological material and aid diagnostic work. The same observations provide a basis for comparing parasite presence across host cells and for relating cellular localization to infection biology.
Drug studies can focus on whether treatment affects amastigote persistence or multiplication within host cells. Because this stage occupies the mammalian intracellular environment, research centered on it can connect antiparasitic activity with the form associated with persistent infection. Such work supports evaluation of candidate treatments for diseases including leishmaniasis and Chagas disease.
They connect kinetoplastid development with persistent infection and disease in both leishmaniasis and Chagas disease. Studying this stage supports investigation of host-pathogen interactions, immune evasion, tissue damage, diagnostic identification, and antiparasitic treatment. Amastigotes therefore provide a shared biological focus while remaining relevant to distinct parasite-host disease settings.