ArticleCritical care medicine2014
C4d deposits on the surface of RBCs in trauma patients and interferes with their function.
Article in Critical care medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- Erythrocytes as immunomodulators in trauma: orchestrating clearance pathways, inflammation, and organ injury.Frontiers in immunology · 2026Review
- Elevated cell-free hemoglobin: A novel early biomarker following traumatic injury.The journal of trauma and acute care surgery · 2025Article
- Complement system activation: bridging physiology, pathophysiology, and therapy.Intensive care medicine · 2024Review
- Articles on hemorrhagic shock published between 2000 and 2021: A CiteSpace-Based bibliometric analysis.Heliyon · 2023Article
- Immunopathology of terminal complement activation and complement C5 blockade creating a pro-survival and organ-protective phenotype in trauma.British journal of pharmacology · 2023Article
- Exploratory Investigation of the Plasma Proteome Associated with the Endotheliopathy of Trauma.International journal of molecular sciences · 2022Article
- Evolution of red blood cell membrane complement regulatory proteins and rheology in septic patients: An exploratory study.Frontiers in medicine · 2022Article
- Genetic and immune crosstalk between severe burns and blunt trauma: A study of transcriptomic data.Frontiers in genetics · 2022Article
- A Review of Complement Activation in SLE.Current rheumatology reports · 2021Review
- Complement Deposition on the Surface of RBC After Trauma Serves a Biomarker of Moderate Trauma Severity: A Prospective Study.Shock (Augusta, Ga.) · 2020Article
- Complement and coagulation cascades in trauma.Acute medicine & surgery · 2019Review
- Innate immune responses to trauma.Nature immunology · 2018Review
- The Epimmunity Theory: The Single Cell Defenses against Infectious and Genetic Diseases.Frontiers in immunology · 2017Article
- Ligation of Glycophorin A Generates Reactive Oxygen Species Leading to Decreased Red Blood Cell Function.PloS one · 2016Article
- Complement, thrombotic microangiopathy and disseminated intravascular coagulation.Journal of intensive care · 2014Review
Corrections and comments
- Commented on by
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveComplement system is activated in patients with trauma. Although complement activation is presumed to contribute to organ damage and constitutional symptoms, little is known about the involved mechanisms. Because complement components may deposit on RBCs, we asked whether complement deposits on the surface of RBC in trauma and whether such deposition alters RBC function.
designA prospective experimental study.
settingResearch laboratory. SUBJECTS: Blood samples collected from 42 trauma patients and 21 healthy donors.
interventionNone. MEASUREMENTS AND MAIN
resultsRBC and sera were collected from trauma patients and control donors. RBCs from trauma patients (n = 40) were found to display significantly higher amounts of C4d on their surface by flow cytometry compared with RBCs from control (n = 17) (p < 0.01). Increased amounts of iC3b were found in trauma sera (n = 27) (vs 12 controls, p < 0.01) by enzyme-linked immunosorbent assay. Incubation of RBC from universal donors (type O, Rh negative) with trauma sera (n = 10) promoted C4d deposition on their surface (vs six controls, p< 0.05). Complement-decorated RBC (n = 6) displayed limited their deformability (vs six controls, p < 0.05) in two-dimensional microchannel arrays. Incubation of RBC with trauma sera (n = 10) promoted the phosphorylation of band 3, a cytoskeletal protein important for the function of the RBC membrane (vs eight controls, p < 0.05), and also accelerated calcium influx (n = 9) and enhanced nitric oxide production (n = 12) (vs four and eight controls respectively, p < 0.05) in flow cytometry.
conclusionsOur study found the presence of extensive complement activation in trauma patients and presents new evidence in support of the hypothesis that complement activation products deposit on the surface of RBC. Such deposition could limit RBC deformability and promote the production of nitric oxide. Our findings suggest that RBC in trauma patients malfunctions, which may explain organ damage and constitutional symptoms that is not accounted for otherwise by previously known pathophysiologic mechanisms.
Indexed as
Identifiers
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.