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Cited by 169Antifungal resistance and susceptibilityFungal Infections and StudiesIron Metabolism and Disorders

Iron Overload Alters Innate and T Helper Cell Responses to Candida albicans in Mice

Mencacci, Antonella, Cenci, Elio, Boelaert, Johan R., Bucci, Paola, Mosci, Paolo, d'Ostiani, Cristiana Fè, Bistoni, Francesco, Romani, Luigina·1997·The Journal of Infectious Diseases
DOI 10.1086/516481
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Abstract

The effect of iron overload on susceptibility of mice to Candida albicans infection and on the type of T helper (Th) immunity elicited was investigated. Iron overload greatly increased susceptibility to disseminated infection with low-virulence C. albicans cells of exogenous origin. The candidacidal activity and the ability to release nitric oxide and bioactive interleukin (IL)-12 were greatly impaired in neutrophils and macrophages from infected mice. CD4 T cells from spleens of iron-overloaded mice were found to produce high levels of IL-4 and IL-10 and low levels of interferon-gamma. Treatment of iron-overloaded mice with the iron chelator, deferoxamine, resulted in the cure of mice from infection, restored the antifungal effector and immunomodulatory functions of the phagocytic cells, and allowed the occurrence of CD4 Th1 protective antifungal responses. These data indicate that iron overload may negatively affect CD4 Th1 development in mice with candidiasis, a function efficiently restored by therapy with deferoxamine.

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Crossref · 10.1086/516481

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  • Immune control of Candida infection could be restored by the iron chelator deferoxamine (DFO).

    “However, immune control of Candida infection could be restored by the iron chelator deferoxamine (DFO) (Mencacci et al., 1997).”

    From Iron in infection and immunity (2020) · cites this paper as Mencacci et al., 1997

    The discussion reports that DFO completely restored resistance to Candida infection and protective immune functions in iron-overloaded mice. The claim omits that condition: the infection-results section says DFO did not change the course or outcome of infection in mice that had not received iron. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Macrophages loaded with iron lose their ability to clear infections with intracellular pathogens, such as Salmonella, Mycobacteria, Chlamydia, Candida, or Legionella.

    “Thus, macrophages loaded with iron lose their ability to clear infections with intracellular pathogens, such as Salmonella, Mycobacteria, Chlamydia, Candida, or Legionella (Mencacci et al., 1997; Chlosta et al., 2006; Nairz et al., 2007; Paradkar et al., 2008; Botella et al., 2012; Bellmann-Weiler et al., 2013) whereas reduction of iron levels or addition of iron chelators can improve infection”

    From Iron at the interface of immunity and infection (2014) · cites this paper as Mencacci et al., 1997

    The Results section reports that iron treatment greatly reduced macrophages’ candidacidal activity, and the Abstract reports increased susceptibility to Candida albicans infection in mice. This supports the Candida example, but the paper reports reduced—not lost—activity and does not establish that macrophages could no longer clear the infection. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Iron overload in mice can hamper the protective Th1 response and the ability to clear C. albicans infection.

    “Iron overload in mice can hamper the protective Th1 response and ability to clear C. albicans infection (Mencacci et al., 1997; Ishida and Johansen, 2014).”

    From Iron at the Centre of Candida albicans Interactions (2018) · cites this paper as Mencacci et al., 1997

  • This pathway appears to be partly responsible for the beneficial clinical effects of iron chelators observed in several experimental infection systems.

    “This pathway appears to be partly responsible for the beneficial clinical effects of iron chelators observed in several experimental infection systems (Mencacci et al., 1997; Fritsche et al., 2001; Ibrahim et al., 2007; Bellmann-Weiler et al., 2013; Nairz et al., 2013).”

    From Iron at the interface of immunity and infection (2014) · cites this paper as Mencacci et al., 1997

  • Inhibition of TFR affects the proliferation of T cell subtypes differently with TH1 immune responses being more sensitive to intracellular iron depletion than TH2.

    “Inhibition of TFR affects the proliferation of T cell subtypes differently with TH1 immune responses being more sensitive to intracellular iron depletion than TH2 (Thorson et al., 1991; Mencacci et al., 1997).”

    From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Mencacci et al., 1997

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Cites

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1 of the 57 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Romani L, Mencacci A, Cenci E, et al. Impaired neutrophil response and CD4 / Th1 development in IL-6 -deficient mice infected with Candida Whatever the mechanisms through which iron regulates Th albicans. J Exp Med 1996; 183:1345 -55.

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Authors
Mencacci, A., Cenci, E., Boelaert, J. R., Bucci, P., Mosci, P., d'Ostiani, C. F., Bistoni, F., & Romani, L.
Affiliations
University of Perugia (IT)
ORCID
Venue
The Journal of Infectious Diseases
Publisher
Oxford University Press (OUP)
Published
1997-06
Volume
175
Issue
6
Pages
1467-1476
ISSN
  • 0022-1899 (ISSN-L)
  • 1537-6613
DOI
10.1086/516481
OpenAlex
W2150374661
Semantic Scholar
599845e36faeaa77f8bb9150b69754059dcae780
Cited by
169
References
57
Citations by year
2026: 3 · 2025: 5 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 6 · 2020: 10 · 2019: 4 · 2018: 6 · 2017: 3 · 2016: 6 · 2015: 7 · 2014: 4 · 2013: 9 · 2012: 8
FWCI
6.44
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Infectious Diseases (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Keywords
iron overload, Candida albicans, candidiasis, deferoxamine, iron chelation, Th1 cells, CD4+ T cells, neutrophils, macrophages, nitric oxide, IL-12, IL-4, IL-10, interferon-gamma, antifungal immunity, disseminated fungal infection, immunomodulation
MeSH terms
Animals, Candida albicans, Candidiasis, Deferoxamine, Disease Susceptibility, Ferric Compounds, Immunoglobulin E, Iron, Iron Chelating Agents, Kidney, Liver, Macrophages, Mice, Inbred BALB C, Neutrophils, Nitrates, Nitric Oxide, RNA, Gene Expression, Cytokines, Th1 Cells, Nitric Oxide Synthase, Iron Overload, Mice

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