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Iron Metabolism and Inflammation
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Iron Metabolism and Inflammation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (10 March 2023) | Viewed by 4891

Special Issue Editors

Dr. Violetta Borelli

E-Mail Website
Guest Editor
Department of Life Sciences, University of Trieste, Via Valerio 28/1, 34127 Trieste, Italy
Interests: asbestos; iron metabolism; hephaestin; mesothelioma; lung cancer; mast cells; neutrophils; inflammation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Giuliano Zabuchi

E-Mail Website
Guest Editor
Department of Life Sciences, University of Trieste, Via Valerio 28/1, 34127 Trieste, Italy
Interests: mast cells; myeloperoxidase; peroxidase; hydrogen peroxide

Special Issue Information

Dear Colleagues,

Iron and its homeostasis are strongly involved in host defence and the inflammatory response. The relationships between iron status and infectious diseases are well documented, with iron deficiency conferring a relative resistance to infection and iron overload promoting its progression. However many aspects of the struggle for iron between microorganisms and host, such as the impact of iron status on inflammatory cells during infection remain unexplained. Indeed iron containing molecules can modulate the function of inflammatory cells. Heme, for example, is per se cytotoxic via ROS production, exerts proinflammatory activity, being a TLR4 ligand and can activate monocytes to M1 or M2 phenotype. Furthermore, ferritin beside to its antioxidant and iron storage role,  may become cytotoxic, promote apoptosis and immunosuppression. Many aspects of  these antithetic events, deserve to be further investigated.

Also chronic inflammatory diseases (eg. atherosclerosis, diabetes, neurodegeneration …) are influenced by iron status which modulation represents a promising  potential therapy target.  For example iron might impact atherosclerosis precisely  through its effects on macrophages, acting in particular at the level of the hepcidin-ferroportin axis. Anyway further research is needed to understand the role of hepcidin in pathways beyond iron metabolism that contribute to atherosclerosis.

In this very complex scenario, the researchers’ effort should trend to obtain progressively a unified  view. Thus, this Special Issue entitled ‘Iron Metabolism and Inflammation’ will discuss the recent advances in molecular mechanisms that involve iron during acute and chronic inflammation and their potential impact as therapeutic targets.

Dr. Violetta Borelli
Prof. Dr. Giuliano Zabuchi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • iron
  • metabolism
  • hepcidin-ferroportin axis
  • hephaestin
  • ferritin
  • infection
  • inflammatory cells
  • metabolic disease
  • neurodegeneration
  • atherosclerosis

Published Papers (2 papers)

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Research

18 pages, 2139 KiB  
Article
Availability of Ferritin-Bound Iron to Enterobacteriaceae
by Clemens M. Gehrer, Alexander Hoffmann, Richard Hilbe, Philipp Grubwieser, Anna-Maria Mitterstiller, Heribert Talasz, Ferric C. Fang, Esther G. Meyron-Holtz, Sarah H. Atkinson, Günter Weiss and Manfred Nairz
Int. J. Mol. Sci. 2022, 23(21), 13087; https://doi.org/10.3390/ijms232113087 - 28 Oct 2022
Cited by 4 | Viewed by 1847
Abstract
The sequestration of iron in case of infection, termed nutritional immunity, is an established strategy of host defense. However, the interaction between pathogens and the mammalian iron storage protein ferritin is hitherto not completely understood. To better characterize the function of ferritin in [...] Read more.
The sequestration of iron in case of infection, termed nutritional immunity, is an established strategy of host defense. However, the interaction between pathogens and the mammalian iron storage protein ferritin is hitherto not completely understood. To better characterize the function of ferritin in Gram-negative infections, we incubated iron-starved cultures of Salmonella Typhimurium and knockout mutant strains defective for major iron uptake pathways or Escherichia coli with horse spleen ferritin or ionic iron as the sole iron source. Additionally, we added bovine superoxide dismutase and protease inhibitors to the growth medium to assess the effect of superoxide and bacterial proteases, respectively, on Salmonella proliferation and reductive iron release. Compared to free ionic iron, ferritin-bound iron was less available to Salmonella, but was still sufficient to significantly enhance the growth of the bacteria. In the absence of various iron acquisition genes, the availability of ferritin iron further decreased. Supplementation with superoxide dismutase significantly reduced the growth of the ΔentC knockout strain with holoferritin as the sole iron source in comparison with ionic ferrous iron. In contrast, this difference was not observed in the wildtype strain, suggesting that superoxide dismutase undermines bacterial iron uptake from ferritin by siderophore-independent mechanisms. Ferritin seems to diminish iron availability for bacteria in comparison to ionic iron, and its iron sequestering effect could possibly be enhanced by host superoxide dismutase activity. Full article
(This article belongs to the Special Issue Iron Metabolism and Inflammation)
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26 pages, 44018 KiB  
Article
Iron Deposition and Ferroptosis in the Spleen in a Murine Model of Acute Radiation Syndrome
by W. Bradley Rittase, John E. Slaven, Yuichiro J. Suzuki, Jeannie M. Muir, Sang-Ho Lee, Milan Rusnak, Grace V. Brehm, Dmitry T. Bradfield, Aviva J. Symes and Regina M. Day
Int. J. Mol. Sci. 2022, 23(19), 11029; https://doi.org/10.3390/ijms231911029 - 20 Sep 2022
Cited by 6 | Viewed by 2389
Abstract
Total body irradiation (TBI) can result in death associated with hematopoietic insufficiency. Although radiation causes apoptosis of white blood cells, red blood cells (RBC) undergo hemolysis due to hemoglobin denaturation. RBC lysis post-irradiation results in the release of iron into the plasma, producing [...] Read more.
Total body irradiation (TBI) can result in death associated with hematopoietic insufficiency. Although radiation causes apoptosis of white blood cells, red blood cells (RBC) undergo hemolysis due to hemoglobin denaturation. RBC lysis post-irradiation results in the release of iron into the plasma, producing a secondary toxic event. We investigated radiation-induced iron in the spleens of mice following TBI and the effects of the radiation mitigator captopril. RBC and hematocrit were reduced ~7 days (nadir ~14 days) post-TBI. Prussian blue staining revealed increased splenic Fe3+ and altered expression of iron binding and transport proteins, determined by qPCR, western blotting, and immunohistochemistry. Captopril did not affect iron deposition in the spleen or modulate iron-binding proteins. Caspase-3 was activated after ~7–14 days, indicating apoptosis had occurred. We also identified markers of iron-dependent apoptosis known as ferroptosis. The p21/Waf1 accelerated senescence marker was not upregulated. Macrophage inflammation is an effect of TBI. We investigated the effects of radiation and Fe3+ on the J774A.1 murine macrophage cell line. Radiation induced p21/Waf1 and ferritin, but not caspase-3, after ~24 h. Radiation ± iron upregulated several markers of pro-inflammatory M1 polarization; radiation with iron also upregulated a marker of anti-inflammatory M2 polarization. Our data indicate that following TBI, iron accumulates in the spleen where it regulates iron-binding proteins and triggers apoptosis and possible ferroptosis. Full article
(This article belongs to the Special Issue Iron Metabolism and Inflammation)
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