The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Cytokine-mediated regulation of iron transport in human monocytic cells
Abstract
Under chronic inflammatory conditions cytokines induce a diversion of iron traffic, leading to hypoferremia and retention of the metal within the reticuloendothelial system. However, the regulatory pathways underlying these disturbances of iron homeostasis are poorly understood. We investigated transferrin receptor (TfR)–dependent and –independent iron transport mechanisms in cytokine-stimulated human monocytic cell lines THP-1 and U937. Combined treatment of cells with interferon-γ (IFN-γ) and lipopolysaccharide (LPS) reduced TfR mRNA levels, surface expression, and iron uptake, and these effects were reversed by interleukin-10 (IL-10), thus stimulating TfR-mediated iron acquisition. IFN-γ and LPS dose-dependently increased the cellular expression of divalent metal transporter-1, a transmembrane transporter of ferrous iron, and stimulated the uptake of nontransferrin bound iron (NTBI) into cells. At the same time, IFN-γ and LPS down-regulated the expression of ferroportin mRNA, a putative iron exporter, and decreased iron release from monocytes. Preincubation with IL-10 partly counteracted these effects. Our results demonstrate that the proinflammatory stimuli IFN-γ and LPS increase the uptake of NTBI via stimulation of divalent metal transporter-1 expression and cause retention of the metal within monocytes by down-regulating ferroportin synthesis. Opposite, the anti-inflammatory cytokine IL-10 stimulates TfR-mediated iron uptake into activated monocytes. The regulation of iron transport by cytokines is a key mechanism in the pathogenesis of anemia of chronic disease and a promising target for therapeutic intervention.
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In the citing paper
“During infections, pro-inflammatory cytokines play an essential role in hepcidin-independent sequestration of iron. Tumour necrosis factor alpha (TNF-α), interleukins (IL-1 and IL-6), and interferon gamma (IFN-γ) increase uptake of free iron by macrophages and transferrin through upregulation of transferrin receptor proteins (Byrd and Horwitz, 1993; Ludwiczek et al., 2003; Drakesmith and Prentice,”
From Iron at the Centre of Candida albicans Interactions (2018) · cites this paper as Ludwiczek et al., 2003
In the citing paper
“Several of these, including TNF, IL-1, IL-6, IL-10 and IL-22 are known as modifiers of iron homeostasis (Armitage et al., 2011;Ludwiczek et al., 2003;Tilg et al., 2002;Torti and Torti, 2002;Weiss, 2005).”
From Iron in infection and immunity (2020) · cites this paper as Ludwiczek et al., 2003
In the citing paper
“TNF, IFN-γ and IL-10 also stimulate the expression of DMT1 and TFR1 thus increasing the uptake of NTBI and TBI by macrophages (Ludwiczek et al., 2003).”
From Iron in infection and immunity (2020) · cites this paper as Ludwiczek et al., 2003
In the citing paper
“In parallel, FPN1 levels are also reduced by transcriptional downregulation, which limits macrophage iron export and fosters iron storage in the cytoplasm (Ludwiczek et al., 2003;Yang et al., 2002).”
From Iron in infection and immunity (2020) · cites this paper as Ludwiczek et al., 2003
In the citing paper
“M2 cytokines like IL-10 - which are virtually absent in the proinflammatory M1 macrophages in nonhealing CVUs - are responsible for the release of iron from the macrophage to the extracellular space”
From An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice (2011) · cites this paper as [58]
In the citing paper
“proinflammatory cytokines released at high concentrations from the unrestrained proinflammatory M1 macrophages further enhance the uptake and intracellular iron retention in macrophages by the induction of transmembrane transporter-1 expression”
From An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice (2011) · cites this paper as [58]
In the citing paper
“Macrophage iron content is further expanded via an inhibitory effect of IFN-γ and LPS on ferroportin transcription thereby reducing cellular iron egress (Yang et al., 2002; Ludwiczek et al., 2003).”
From Iron at the interface of immunity and infection (2014) · cites this paper as Ludwiczek et al., 2003
In the citing paper
“DMT1 expression and iron transport capacity are increased in inflammatory MΦs (245); however, it has not been investigated whether this is also paralleled by increased accumulation of copper, zinc, or manganese in macrophages and whether or not this strengthens anti-microbial activities against M. tuberculosis.”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [245]
In the citing paper
“In the circulation there is also non-transferrin bound iron (NTBI) which can be taken up into the cell by ZIP- (ZRT/IRT-like protein)-14 or DMT1 (Ludwiczek et al., 2003; Liuzzi et al., 2006; Pinilla-Tenas et al., 2011; Figure 1);”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Ludwiczek et al., 2003
In the citing paper
“IFNγ has a strong regulatory role in iron homeostasis as it enhances the expression of cellular iron-regulating genes such as HO-1 but also reduces the iron-exporting gene ferroportin (Ludwiczek et al., 2003; Nairz et al., 2015).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Ludwiczek et al., 2003
In the citing paper
“Tfr1, which is also known as CD71, is widely expressed by isolated macrophages, and it may form a major route of iron uptake in the absence of RBC (an indirect iron source), though it also appears to be important in adaptive immunity [103, 138].”
From “Pumping iron”—how macrophages handle iron at the systemic, microenvironmental, and cellular levels (2017) · cites this paper as [138]
In the citing paper
“Specifically, macrophage functions driven by IFN-γ are impaired when macrophages are exposed to surplus iron [138, 162, 176] largely because iron directly inhibits the binding activities of the transcription factors nuclear factor interleukin-6 (NF-IL6) and hypoxia-inducible factor (HIF)-1α [55, 153] [176].”
From “Pumping iron”—how macrophages handle iron at the systemic, microenvironmental, and cellular levels (2017) · cites this paper as [138]
In the citing paper
“Reduction in intracellular iron concentrations has been shown to promote the production of pro-inflammatory molecules such as TNF-α, IL-6, iNOS (nos2) or CCL-20 by activated macrophages (Weiss et al., 1994; Melillo et al., 1997; Ludwiczek et al., 2003; Oexle et al., 2003; Varesio et al., 2010), and these pathways are of importance for the control of intracellular pathogens like Salmonella (Andrews”
From Heme oxygenase 1 controls early innate immune response of macrophages to Salmonella Typhimurium infection: Heme oxygenase 1 expression affects Salmonella infection (2016) · cites this paper as Ludwiczek et al., 2003
In the citing paper
“It is noteworthy that several cytokines impact on iron homeostasis mainly in macrophages by non-hepcidin mediated pathways thereby increasing iron uptake via different pathways but also by reducing erythrocyte half-life with subsequent stimulation of erythrophagocytosis, by promotion of iron storage within ferritin and by reduction cellular iron egress [172][173][174][175][176][177][178][179].”
From Iron in immune cell function and host defense (2021) · cites this paper as [174]
In the citing paper
“Inflammation-driven Hamp induction thus causes iron sequestration within the mononuclear phagocyte system (MPS), which limits iron availability for extracellular pathogens (Bridle et al., 2003; Ludwiczek et al., 2003; Ganz, 2005; Theurl et al., 2008a).”
From Genetic and Dietary Iron Overload Differentially Affect the Course of Salmonella Typhimurium Infection (2017) · cites this paper as Ludwiczek et al., 2003
In the citing paper
“For instance, lipopolysaccharide as a component of the Gram-negative cell wall enhances HAMP production while stimulating DMT1 expression in myeloid cells, thereby favoring iron sequestration [35].”
From Iron deficiency or anemia of inflammation?: Differential diagnosis and mechanisms of anemia of inflammation (2016) · cites this paper as [35]
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Metadata
- Authors
- Ludwiczek, S., Aigner, E., Theurl, I., & Weiss, G.
- Affiliations
- Innsbruck Medical University (AT)
- From the Department of Internal Medicine, University Hospital, Innsbruck, Austria.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2003-05-15
- Volume
- 101
- Issue
- 10
- Pages
- 4148-4154
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2066929242
- Cited by
- 420
- References
- 56
- Citations by year
- 2026: 12 · 2025: 4 · 2024: 7 · 2023: 14 · 2022: 16 · 2021: 22 · 2020: 23 · 2019: 16 · 2018: 19 · 2017: 15 · 2016: 11 · 2015: 16 · 2014: 23 · 2013: 25 · 2012: 26
- FWCI
- 10.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
- Keywords
- iron homeostasis, cytokines, iron transport, transferrin receptor, interferon-gamma, lipopolysaccharide, IL-10, DMT1, ferroportin, non-transferrin-bound iron, monocytes, THP-1 cells, U937 cells, anemia of chronic disease, inflammation
- MeSH terms
- Ferroportin, Solute Carrier Family 11, Member 2, Base Sequence, Biological Transport, Humans, Interferon-gamma, Iron, Kinetics, Lipopolysaccharides, Monocytes, Receptors, Transferrin, Tumor Cells, Cultured, Polymerase Chain Reaction, Cytokines, Interleukin-10, DNA Primers, U937 Cells, Cation Transport Proteins, Iron-Binding Proteins
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