The marsupial trypanosome Trypanosoma copemani is not an obligate intracellular parasite, although it adversely affects cell health

Crystal Cooper, R. C. Andrew Thompson, Paul Rigby, Alysia Buckley, Christopher Peacock, Peta L. Clode

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Abstract

Background: Trypanosoma cruzi invades and replicates inside mammalian cells, which can lead to chronic Chagas disease in humans. Trypanosoma copemani infects Australian marsupials and recent investigations indicate it may be able to invade mammalian cells in vitro, similar to T. cruzi. Here, T. cruzi 10R26 strain (TcIIa) and two strains of T. copemani [genotype 1 (G1) and genotype 2 (G2)] were incubated with marsupial cells in vitro. Live-cell time-lapse and fluorescent microscopy, combined with high-resolution microscopy (transmission and scanning electron microscopy) were used to investigate surface interactions between parasites and mammalian cells. Results: The number of parasites invading cells was significantly higher in T. cruzi compared to either genotype of T. copemani, between which there was no significant difference. While capable of cellular invasion, T. copemani did not multiply in host cells in vitro as there was no increase in intracellular amastigotes over time and no release of new trypomastigotes from host cells, as observed in T. cruzi. Exposure of host cells to G2 trypomastigotes resulted in increased host cell membrane permeability within 24 h of infection, and host cell death/blebbing was also observed. G2 parasites also became embedded in the host cell membrane. Conclusions: Trypanosoma copemani is unlikely to have an obligate intracellular life-cycle like T. cruzi. However, T. copemani adversely affects cell health in vitro and should be investigated in vivo in infected host tissues to better understand this host-parasite relationship. Future research should focus on increasing understanding of the T. copemani life history and the genetic, physiological and ecological differences between different genotypes.

Original languageEnglish
Article number521
JournalParasites and Vectors
Volume11
Issue number1
DOIs
Publication statusPublished - 20 Sep 2018

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Trypanosoma
Marsupialia
Trypanosomiasis
Parasites
Trypanosoma cruzi
Health
Genotype
Microscopy
Cell Membrane Permeability
Host-Parasite Interactions
Scanning Transmission Electron Microscopy
Chagas Disease
Blister
Life Cycle Stages
Chronic Disease
Cell Death
Cell Membrane

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@article{f9af17504d0a4049a7fc0c3d229602e1,
title = "The marsupial trypanosome Trypanosoma copemani is not an obligate intracellular parasite, although it adversely affects cell health",
abstract = "Background: Trypanosoma cruzi invades and replicates inside mammalian cells, which can lead to chronic Chagas disease in humans. Trypanosoma copemani infects Australian marsupials and recent investigations indicate it may be able to invade mammalian cells in vitro, similar to T. cruzi. Here, T. cruzi 10R26 strain (TcIIa) and two strains of T. copemani [genotype 1 (G1) and genotype 2 (G2)] were incubated with marsupial cells in vitro. Live-cell time-lapse and fluorescent microscopy, combined with high-resolution microscopy (transmission and scanning electron microscopy) were used to investigate surface interactions between parasites and mammalian cells. Results: The number of parasites invading cells was significantly higher in T. cruzi compared to either genotype of T. copemani, between which there was no significant difference. While capable of cellular invasion, T. copemani did not multiply in host cells in vitro as there was no increase in intracellular amastigotes over time and no release of new trypomastigotes from host cells, as observed in T. cruzi. Exposure of host cells to G2 trypomastigotes resulted in increased host cell membrane permeability within 24 h of infection, and host cell death/blebbing was also observed. G2 parasites also became embedded in the host cell membrane. Conclusions: Trypanosoma copemani is unlikely to have an obligate intracellular life-cycle like T. cruzi. However, T. copemani adversely affects cell health in vitro and should be investigated in vivo in infected host tissues to better understand this host-parasite relationship. Future research should focus on increasing understanding of the T. copemani life history and the genetic, physiological and ecological differences between different genotypes.",
keywords = "Australia, Host-parasite interactions, Marsupials, Trypanosoma copemani, Trypanosoma cruzi",
author = "Crystal Cooper and {Andrew Thompson}, {R. C.} and Paul Rigby and Alysia Buckley and Christopher Peacock and Clode, {Peta L.}",
year = "2018",
month = "9",
day = "20",
doi = "10.1186/s13071-018-3092-1",
language = "English",
volume = "11",
journal = "PARASITES & VECTORS",
issn = "1756-3305",
publisher = "BioMed Central",
number = "1",

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TY - JOUR

T1 - The marsupial trypanosome Trypanosoma copemani is not an obligate intracellular parasite, although it adversely affects cell health

AU - Cooper, Crystal

AU - Andrew Thompson, R. C.

AU - Rigby, Paul

AU - Buckley, Alysia

AU - Peacock, Christopher

AU - Clode, Peta L.

PY - 2018/9/20

Y1 - 2018/9/20

N2 - Background: Trypanosoma cruzi invades and replicates inside mammalian cells, which can lead to chronic Chagas disease in humans. Trypanosoma copemani infects Australian marsupials and recent investigations indicate it may be able to invade mammalian cells in vitro, similar to T. cruzi. Here, T. cruzi 10R26 strain (TcIIa) and two strains of T. copemani [genotype 1 (G1) and genotype 2 (G2)] were incubated with marsupial cells in vitro. Live-cell time-lapse and fluorescent microscopy, combined with high-resolution microscopy (transmission and scanning electron microscopy) were used to investigate surface interactions between parasites and mammalian cells. Results: The number of parasites invading cells was significantly higher in T. cruzi compared to either genotype of T. copemani, between which there was no significant difference. While capable of cellular invasion, T. copemani did not multiply in host cells in vitro as there was no increase in intracellular amastigotes over time and no release of new trypomastigotes from host cells, as observed in T. cruzi. Exposure of host cells to G2 trypomastigotes resulted in increased host cell membrane permeability within 24 h of infection, and host cell death/blebbing was also observed. G2 parasites also became embedded in the host cell membrane. Conclusions: Trypanosoma copemani is unlikely to have an obligate intracellular life-cycle like T. cruzi. However, T. copemani adversely affects cell health in vitro and should be investigated in vivo in infected host tissues to better understand this host-parasite relationship. Future research should focus on increasing understanding of the T. copemani life history and the genetic, physiological and ecological differences between different genotypes.

AB - Background: Trypanosoma cruzi invades and replicates inside mammalian cells, which can lead to chronic Chagas disease in humans. Trypanosoma copemani infects Australian marsupials and recent investigations indicate it may be able to invade mammalian cells in vitro, similar to T. cruzi. Here, T. cruzi 10R26 strain (TcIIa) and two strains of T. copemani [genotype 1 (G1) and genotype 2 (G2)] were incubated with marsupial cells in vitro. Live-cell time-lapse and fluorescent microscopy, combined with high-resolution microscopy (transmission and scanning electron microscopy) were used to investigate surface interactions between parasites and mammalian cells. Results: The number of parasites invading cells was significantly higher in T. cruzi compared to either genotype of T. copemani, between which there was no significant difference. While capable of cellular invasion, T. copemani did not multiply in host cells in vitro as there was no increase in intracellular amastigotes over time and no release of new trypomastigotes from host cells, as observed in T. cruzi. Exposure of host cells to G2 trypomastigotes resulted in increased host cell membrane permeability within 24 h of infection, and host cell death/blebbing was also observed. G2 parasites also became embedded in the host cell membrane. Conclusions: Trypanosoma copemani is unlikely to have an obligate intracellular life-cycle like T. cruzi. However, T. copemani adversely affects cell health in vitro and should be investigated in vivo in infected host tissues to better understand this host-parasite relationship. Future research should focus on increasing understanding of the T. copemani life history and the genetic, physiological and ecological differences between different genotypes.

KW - Australia

KW - Host-parasite interactions

KW - Marsupials

KW - Trypanosoma copemani

KW - Trypanosoma cruzi

UR - http://www.scopus.com/inward/record.url?scp=85055130385&partnerID=8YFLogxK

U2 - 10.1186/s13071-018-3092-1

DO - 10.1186/s13071-018-3092-1

M3 - Article

VL - 11

JO - PARASITES & VECTORS

JF - PARASITES & VECTORS

SN - 1756-3305

IS - 1

M1 - 521

ER -