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Cited by 60Trypanosoma species research and implicationsIron Metabolism and DisordersResearch on Leishmaniasis Studies

The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.

Role of iron in intracellular growth of Trypanosoma cruzi

Open access
Loo, V G, Lalonde, R G·1984·Infection and Immunity
DOI 10.1128/iai.45.3.726-730.1984PMC PMC263357
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Abstract

Host hypoferremic responses occur during infection with Trypanosoma cruzi, presumably through the transfer of iron to the sites of intracellular parasite replication. Depletion of host intracellular iron stores reduces parasite pathogenicity. It has therefore been hypothesized that T. cruzi requires iron for optimal growth in host cells and that, unlike extracellular pathogens, T. cruzi may benefit from host hypoferremic responses. These hypotheses were examined by the in vitro infection of peritoneal macrophages with T. cruzi. Various doses of desferrioxamine or referrated desferrioxamine were added to the culture medium, and parasite growth was monitored. The influence of treatment on uninfected macrophage morphology, function, and iron content was also verified. Desferrioxamine reduced the rate of amastigote replication in a dose-dependent fashion, whereas referrated desferrioxamine did not. The iron content of desferrioxamine-treated macrophages was decreased by 55% without provoking significant morphological or functional changes. Thus, amastigotes used host cell iron stores for optimal growth, and desferrioxamine reduced growth by depleting host cell iron. Hence, it was suggested that depletion of host intracellular iron stores may protect against T. cruzi and, furthermore, that host responses which transfer iron to the intracellular sites of T. cruzi replication may enhance parasite pathogenicity.

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Crossref · 10.1128/iai.45.3.726-730.1984

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  • The T. cruzi genome does not contain an obvious LIT1 orthologue.

    “Intriguingly, the T. cruzi genome does not contain an obvious LIT1 orthologue, raising the possibility that this Fe2+-transporter represents a specific Leishmania adaptation to the low Fe environment of phagolysosomes [88].”

    From Strategies of intracellular pathogens for obtaining iron from the environment (2015) · cites this paper as [88]

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Metadata

Authors
Loo, V. G., & Lalonde, R. G.
ORCID
Loo, V G
Venue
Infection and Immunity
Publisher
American Society for Microbiology
Published
1984-09
Volume
45
Issue
3
Pages
726-730
ISSN
  • 0019-9567 (ISSN-L)
  • 1098-5522
DOI
10.1128/iai.45.3.726-730.1984
PMC
PMC263357
OpenAlex
W2171060765
Cited by
60
References
13
Citations by year
2026: 1 · 2023: 1 · 2022: 1 · 2020: 4 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 1 · 2013: 2 · 2012: 3
FWCI
0.85
Type
journal article
Language
en
Open access
Licence
journals.asm.org/non-commercial-tdm-license (tdm)
Locations
  • Infection and Immunity (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Trypanosoma species research and implications
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Research on Leishmaniasis Studies
Keywords
Trypanosoma cruzi, Chagas disease, iron metabolism, deferoxamine, peritoneal macrophages, host-parasite interactions, parasite pathogenicity
MeSH terms
Animals, Cells, Cultured, Deferoxamine, Iron, Macrophages, Trypanosoma cruzi, Mice

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