Hemopexin therapy reverts heme-induced proinflammatory phenotypic switching of macrophages in a mouse model of sickle cell disease
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Key Points: Heme and iron induce macrophage phenotypic switching toward an M1 proinflammatory phenotype. By scavenging free heme, hemopexin reverts heme-induced proinflammatory activation of macrophages in a mouse model of sickle cell disease.
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Iron present in heme can stimulate production of ROS and pro-inflammatory cytokines such as TNF, IL-1ß, and IL-6.
“In this context, iron present in heme can stimulate the production of ROS and of pro-inflammatory cytokines such as TNF, IL-1ß, and IL-6 [241].”
From “Pumping iron”—how macrophages handle iron at the systemic, microenvironmental, and cellular levels (2017) · cites this paper as [241]
The iron species used and route of uptake are not crucial for macrophage polarization outcome, as heme and simple iron chelates can also induce a phenotypical shift.
“Vinchi and colleagues showed that the iron species used and the route of uptake is not crucial for the outcome of macrophage polarization, as evidenced by the fact that also even heme and simple iron chelates can induce a phenotypical shift in macrophages [215].”
From Iron oxide nanoparticles: Diagnostic, therapeutic and theranostic applications (2019) · cites this paper as [215]
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- Authors
- Vinchi, F., Costa da Silva, M., Ingoglia, G., Petrillo, S., Brinkman, N., Zuercher, A., Cerwenka, A., Tolosano, E., & Muckenthaler, M. U.
- Affiliations
- Heidelberg University (DE)
- Department of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg, Germany;
- University of Turin (IT)
- CSL Behring, Research & Development, Kankakee, IL; and
- CSL (Switzerland) (CH)
- German Cancer Research Center (DE)
- Corresponding author
- Vinchi, Francesca
- Tolosano, Emanuela
- Muckenthaler, Martina U.
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2016-01-28
- Volume
- 127
- Issue
- 4
- Pages
- 473-486
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC4850229
- OpenAlex
- W2405628819
- Cited by
- 269
- References
- 73
- Citations by year
- 2026: 15 · 2025: 12 · 2024: 28 · 2023: 29 · 2022: 27 · 2021: 36 · 2020: 31 · 2019: 31 · 2018: 25 · 2017: 23 · 2016: 12
- FWCI
- 11.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
- Funders
- CSL Behring
- Deutsche Forschungsgemeinschaft
- Universität Heidelberg
- Università degli Studi di Verona
- Topics
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hemoglobin structure and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heme Oxygenase-1 and Carbon Monoxide
- Keywords
- hemopexin, sickle cell disease, inflammatory macrophages, hepatic macrophages, reticuloendothelial system, reactive oxygen species, TLR4 signaling, heme scavenging, chronic inflammation, hemolysis, iron overload
- MeSH terms
- Anemia, Sickle Cell, Animals, Anti-Inflammatory Agents, Cell Line, Cells, Cultured, Disease Models, Animal, Heme, Hemopexin, Humans, Macrophages, Cytokines, Gene Deletion, Reactive Oxygen Species, Mice, Knockout, Toll-Like Receptor 4, Mice
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