ArticleThe Journal of biological chemistry2015
Commensal Bacteria-induced Interleukin 1β (IL-1β) Secreted by Macrophages Up-regulates Hepcidin Expression in Hepatocytes by Activating the Bone Morphogenetic Protein Signaling Pathway.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Pooled it
- Animal models of anemia of inflammation: Methodological advances, limitations, and translational applications.Animal models and experimental medicine · 2026Review
- The Gut-Iron-Immune Axis in Severe Anaemia and Bacteraemia.Nutrients · 2026Review
- Iron Dysregulation and Vascular Diseases: A Contemporary Review.Journal of the American Heart Association · 2026Review
- The role of hepcidin in the inflammatory and iron homeostasis axis in inflammatory bowel diseases: a systematic review.Translational gastroenterology and hepatology · 2026Review
- Article
- Crosstalk Between Microbiome and Ferroptosis in Diseases: From Mechanism to Therapy.Comprehensive Physiology · 2025Review
- Hepatocyte Toll-like receptors contribute to the hepcidin inflammatory response to pathogens and pathogen-derived ligands.HemaSphere · 2025Article
- Single-cell transcriptomics and machine learning unveil ferroptosis features in tumor-associated macrophages: Prognostic model and therapeutic strategies for lung adenocarcinoma.Frontiers in pharmacology · 2025Article
- Unveiling the crucial role of ferroptosis in host resistance to streptococcus agalactiae infection.Cell death discovery · 2024Article
- Direct and macrophage stimulation mediated effects of active, inactive, and cell-free supernatant forms of Akkermansia muciniphila and Faecalibacterium duncaniae on hepcidin gene expression in HepG2 cells.Archives of microbiology · 2024Article
- Interplay between gut microbiota and the master iron regulator, hepcidin, in the pathogenesis of liver fibrosis.Pathogens and disease · 2024Review
- The intricate interplay between ferroptosis and efferocytosis in cancer: unraveling novel insights and therapeutic opportunities.Frontiers in oncology · 2024Review
- Stimulation of Hepatic Ferritinophagy MitigatesAntioxidants (Basel, Switzerland) · 2023Article
- Effects of Tocilizumab on Inflammation and Iron Metabolism in Critically Ill Patients with COVID-19.Pharmaceutics · 2023Article
- Inflammatory adipose activates a nutritional immunity pathway leading to retinal dysfunction.Cell reports · 2022Article
- Novel Insights into Alcoholic Liver Disease: Iron Overload, Iron Sensing and Hemolysis.Journal of translational internal medicine · 2022Article
- Interaction between macrophages and ferroptosis.Cell death & disease · 2022Review
- Vascular Calcification: New Insights Into BMP Type I Receptor A.Frontiers in pharmacology · 2022Review
- Crosstalk between liver macrophages and gut microbiota: An important component of inflammation-associated liver diseases.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The liver hormone hepcidin is the central regulator of systemic iron metabolism. Its increased expression in inflammatory states leads to hypoferremia and anemia. Elucidation of the mechanisms that up-regulate hepcidin during inflammation is essential for developing rational therapies for this anemia. Using mouse models of inflammatory bowel disease, we have shown previously that colitis-associated hepcidin induction is influenced by intestinal microbiota composition. Here we investigate how two commensal bacteria, Bifidobacterium longum and Bacteroides fragilis, representative members of the gut microbiota, affect hepcidin expression. We found that supernatants of a human macrophage cell line infected with either of the bacteria up-regulated hepcidin when added to a human hepatocyte cell line. This activity was abrogated by neutralization of IL-1β. Moreover, purified IL-1β increased hepcidin expression when added to the hepatocyte line or primary human hepatocytes and when injected into mice. IL-1β activated the bone morphogenetic protein (BMP) signaling pathway in hepatocytes and in mouse liver, as indicated by increased phosphorylation of small mothers against decapentaplegic proteins. Activation of BMP signaling correlated with IL-1β-induced expression of BMP2 in human hepatocytes and activin B in mouse liver. Treatment of hepatocytes with two different chemical inhibitors of BMP signaling or with a neutralizing antibody to BMP2 prevented IL-1β-induced up-regulation of hepcidin. Our results clarify how commensal bacteria affect hepcidin expression and reveal a novel connection between IL-1β and activation of BMP signaling. They also suggest that there may be differences between mice and humans with respect to the mechanism by which IL-1β up-regulates hepcidin.
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Registered trials
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