ArticleNature immunology2016
Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions.
Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
97 citing papers in PubMed, 141 citations in OpenAlex.
- Haemolytic injury and cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Ferroptosis is a Physiologic Vulnerability of Iron-Recycling Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Hypomorphic biliverdin reductase a mutations define bilirubin anti-malarial threshold.iScience · 2026Article
- Salmonella-derived haem inhibits macrophage phagocytosis and promotes infection in mice.Nature microbiology · 2026Article
- Article
- β-Glucan Protects Against Sepsis-Induced Kupffer Cell Loss by Inhibiting Pyroptosis and Promoting Self-Renewal.Immunology · 2026Article
- DOCK8 in immune cells: roles and mechanisms.Frontiers in immunology · 2026Review
- One trigger, two fates: hemolysate shapes neutrophil extracellular traps (NETs) formation in a context-dependent manner.Frontiers in immunology · 2026Article
- Homeostatic control of energy metabolism by monocyte-derived macrophages.The EMBO journal · 2026Article
- Heme drives cardiac endothelial senescence in sepsis via STING activation.Cell death & disease · 2025Article
- MDM2-P53-V-ATPases axis driven by dehydroevodiamine to fight intracellular bacterial infection.Communications biology · 2025Article
- Heme in Bacterial Pathogenesis and as an Antimicrobial Target.Chemical reviews · 2025Review
- Beyond anemia: unraveling neutrophil defects and infection susceptibility in β-Thalassemia.Blood research · 2025Review
- The role of heme in sepsis induced Kupffer cell PANoptosis and senescence.Cell death & disease · 2025Article
- Article
- Mechanisms of HAHV-1 Interaction with Hemocytes inBiology · 2025Article
- Microbial adaptive pathogenicity strategies to the host inflammatory environment.FEMS microbiology reviews · 2025Review
- Mechanisms and therapeutic potential of disulphidptosis in cancer.Cell proliferation · 2025Review
- CircCDC42-encoded CDC42-165aa regulates macrophage pyroptosis in Klebsiella pneumoniae infection through Pyrin inflammasome activation.Nature communications · 2024Article
- Neutrophils versus Protozoan Parasites:Microorganisms · 2024Review
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
28 authors at 5 institutions in 3 countries.
Funding
Abstract
Hemolysis drives susceptibility to bacterial infections and predicts poor outcome from sepsis. These detrimental effects are commonly considered to be a consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative sepsis model and found that elevated heme levels impaired the control of bacterial proliferation independently of heme-iron acquisition by pathogens. Heme strongly inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach revealed that quinine effectively prevented heme effects on the cytoskeleton, restored phagocytosis and improved survival in sepsis. These mechanistic insights provide potential therapeutic targets for patients with sepsis or hemolytic disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.