ArticleNature medicine2009
Heterotypic interactions enabled by polarized neutrophil microdomains mediate thromboinflammatory injury.
Article in Nature medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02824471 (Sickle Cell Disease), which is not on this map. Cited by 198 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Sickle Cell Disease (SCD) Biochip': Towards a Simple and Reliable Way to Monitor Sickle Cell Disease
Who cites it
198 citing papers in PubMed, 341 citations in OpenAlex.
- Single-dose intravenous gammaglobulin can stabilize neutrophil Mac-1 activation in sickle cell pain crisis.American journal of hematology · 2015Trial
- Beneficial effects of SGLT1/2 and SGLT2 inhibitors on vaso-occlusive events and organ damage in sickle cell disease mice.Cardiovascular research · 2026Article
- A circadian checkpoint relocates neutrophils to minimize injury.The Journal of experimental medicine · 2026Article
- The small-molecule Syk inhibitor R788 inhibits hematopoiesis and worsens anemia in sickle cell disease mice.Blood vessels, thrombosis & hemostasis · 2026Article
- CD39 polymorphism enables lung thrombosis in sickle cell disease.Nature communications · 2026Article
- Mouse Models of Transfusion-Related Acute Lung Injury (TRALI).Methods in molecular biology (Clifton, N.J.) · 2026Article
- Mechanisms That Prevent Vascular Leakage During Leukocyte Extravasation.Acta physiologica (Oxford, England) · 2025Review
- Acute lung injury induced by traumatic hemorrhagic shock: pathogenesis, biomarkers and therapeutic perspectives.World journal of emergency medicine · 2025Article
- Platelets as drivers of immunothrombosis in rheumatic diseases.Nature reviews. Rheumatology · 2025Review
- Crosstalk Between Sickle Cell Disease and Ferroptosis.International journal of molecular sciences · 2025Review
- From Defense to Dysfunction: Decoding the Paradox of Emergency Granulopoiesis in Sepsis Pathogenesis.Research (Washington, D.C.) · 2025Review
- Dynamics of neutrophil phenotype and function in sickle cell disease.Frontiers in immunology · 2025Article
- Neutrophils-biology and diversity.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Review
- Biased agonism of protease-activated receptor-1 regulates thromboinflammation in murine sickle cell disease.Blood advances · 2024Article
- A multicellular vessel-on-a-chip model reveals context-dependent roles for platelets in inflammation and inflammatory hemostasis.Blood vessels, thrombosis & hemostasis · 2024Article
- Immune Cell Migration to Cancer.Cells · 2024Review
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- Circadian Effects on Vascular Immunopathologies.Circulation research · 2024Review
- Neutrophil Extracellular DNA Traps in Response to Infection or Inflammation, and the Roles of Platelet Interactions.International journal of molecular sciences · 2024Review
138 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Selectins and their ligands mediate leukocyte rolling, allowing interactions with chemokines that lead to integrin activation and arrest. Here we show that E-selectin is crucial for generating a secondary wave of activating signals, transduced specifically by E-selectin ligand-1, that induces polarized, activated alpha(M)beta(2) integrin clusters at the leading edge of crawling neutrophils, allowing capture of circulating erythrocytes or platelets. In a humanized mouse model of sickle cell disease, the capture of erythrocytes by alpha(M)beta(2) microdomains leads to acute lethal vascular occlusions. In a model of transfusion-related acute lung injury, polarized neutrophils capture circulating platelets, resulting in the generation of oxidative species that produce vascular damage and lung injury. Inactivation of E-selectin or alpha(M)beta(2) prevents tissue injury in both inflammatory models, suggesting broad implications of this paradigm in thromboinflammatory diseases. These results indicate that endothelial selectins can influence neutrophil behavior beyond its canonical rolling step through delayed, organ-damaging, polarized activation.
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What OpenQuestion holds
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.