ArticleCellular microbiology2013
Extracellular amastigotes of Trypanosoma cruzi are potent inducers of phagocytosis in mammalian cells.
Article in Cellular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- Leishmania amazonensis amastigotes invade non-phagocytic cells via highly localized parasite-induced actin remodeling.PLoS neglected tropical diseases · 2026Article
- The Screen of a Phage Display Library Identifies a Peptide That Binds to the Surface ofFrontiers in microbiology · 2022Article
- All Roads Lead to Cytosol:Frontiers in cellular and infection microbiology · 2021Review
- The Parasitic Intracellular Lifestyle of Trypanosomatids: Parasitophorous Vacuole Development and Survival.Frontiers in cell and developmental biology · 2020Review
- Autophagy: A necessary process during theVirulence · 2019Review
- Host cell protein LAMP-2 is the receptor for Trypanosoma cruzi surface molecule gp82 that mediates invasion.Cellular microbiology · 2019Article
- Utilization of proliferable extracellular amastigotes for transient gene expression, drug sensitivity assay, and CRISPR/Cas9-mediated gene knockout in Trypanosoma cruzi.PLoS neglected tropical diseases · 2019Article
- Host cell perforation by listeriolysin O (LLO) activates a CaMolecular biology of the cell · 2018Article
- Amastigote Synapse: The Tricks ofFrontiers in microbiology · 2018Article
- Rac1/WAVE2 and Cdc42/N-WASP Participation in Actin-Dependent Host Cell Invasion by Extracellular Amastigotes ofFrontiers in microbiology · 2018Article
- A Carbohydrate Moiety of Secreted Stage-Specific Glycoprotein 4 Participates in Host Cell Invasion byFrontiers in microbiology · 2018Article
- ERM Proteins Play Distinct Roles in Cell Invasion by Extracellular Amastigotes ofFrontiers in microbiology · 2017Article
- The N-myristoylome of Trypanosoma cruzi.Scientific reports · 2016Article
- Unique behavior of Trypanosoma cruzi mevalonate kinase: A conserved glycosomal enzyme involved in host cell invasion and signaling.Scientific reports · 2016Article
- Article
- The Dialogue of the Host-Parasite Relationship: Leishmania spp. and Trypanosoma cruzi Infection.BioMed research international · 2015Review
- Mechanisms of cellular invasion by intracellular parasites.Cellular and molecular life sciences : CMLS · 2014Review
- An historical perspective on how advances in microscopic imaging contributed to understanding the Leishmania Spp. and Trypanosoma cruzi host-parasite relationship.BioMed research international · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The protozoan parasite Trypanosoma cruzi, the aetiological agent of Chagas' disease, has two infective life cycle stages, trypomastigotes and amastigotes. While trypomastigotes actively enter mammalian cells, highly infective extracellular amastigotes (type I T. cruzi) rely on actin-mediated uptake, which is generally inefficient in non-professional phagocytes. We found that extracellular amastigotes (EAs) of T. cruzi G strain (type I), but not Y strain (type II), were taken up 100-fold more efficiently than inert particles. Mammalian cell lines showed levels of parasite uptake comparable to macrophages, and extensive actin recruitment and polymerization was observed at the site of entry. EA uptake was not dependent on parasite-secreted molecules and required the same molecular machinery utilized by professional phagocytes during large particle phagocytosis. Transcriptional silencing of synaptotagmin VII and CD63 significantly inhibited EA internalization, demonstrating that delivery of supplemental lysosomal membrane to form the phagosome is involved in parasite uptake. Importantly, time-lapse live imaging using fluorescent reporters revealed phagosome-associated modulation of phosphoinositide metabolism during EA uptake that closely resembles what occurs during phagocytosis by macrophages. Collectively, our results demonstrate that T. cruzi EAs are potent inducers of phagocytosis in non-professional phagocytes, a process that may facilitate parasite persistence in infected hosts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.