ArticleClinical and experimental immunology2018
Blood clotting and traumatic injury with shock mediates complement-dependent neutrophil priming for extracellular ROS, ROS-dependent organ injury and coagulopathy.
Article in Clinical and experimental immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Incidence and factors independently associated with acute respiratory distress syndrome in chinese patients with severe acute pancreatitis: a systematic review and meta-analysis.BMC pulmonary medicine · 2026Pooled it
- Trial
- Loss of C3 and CD14 reduces region-specific neuroinflammation in a murine polytrauma model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The "Double-Edged Sword" of Neutrophils in Trauma: From Pathophysiological Mechanisms to Precision Immunomodulation Strategies.International journal of molecular sciences · 2026Review
- Mitochondria: The Crossroads of Complement Activation and Kidney Injury Progression.International journal of molecular sciences · 2026Review
- Whole blood becomes increasingly susceptible to tPA-mediated fibrinolysis with storage.The journal of trauma and acute care surgery · 2026Article
- Plasminogen supplementation improves lysis of inflammatory retained traumatic hemothorax.The journal of trauma and acute care surgery · 2026Article
- A Targeted Blockade of Terminal C5a Is Critical to Management of Sepsis and Acute Respiratory Distress Syndrome: The Mechanism of Action of Vilobelimab.International journal of molecular sciences · 2025Review
- Tranexamic Acid and Systemic Complement Activation in Traumatic Brain Injury Patients.Journal of the American College of Surgeons · 2025Article
- The important role of preoperative ultrasound in the efficacy and safety of coronary intervention via distal transradial access.BMC cardiovascular disorders · 2025Article
- Preeclamptic Placental CD19+ B Cells Are Causal to Hypertension During Pregnancy.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Dysregulation of neutrophil in sepsis: recent insights and advances.Cell communication and signaling : CCS · 2025Review
- Laboratory and clinical haemostatic aberrations in primary dermatologic disease: A review.Thrombosis journal · 2024Review
- Endogenous and exogenous protection from surgically induced reactive oxygen and nitrogen species.Surgery today · 2024Review
- New insight of complement system in the process of vascular calcification.Journal of cellular and molecular medicine · 2023Review
- Immunopathology of terminal complement activation and complement C5 blockade creating a pro-survival and organ-protective phenotype in trauma.British journal of pharmacology · 2023Article
- Article
- Proteomics of Coagulopathy Following Injury Reveals Limitations of Using Laboratory Assessment to Define Trauma-Induced Coagulopathy to Predict Massive Transfusion.Annals of surgery open : perspectives of surgical history, education, and clinical approaches · 2022Article
- Antioxidants as Therapeutic Agents in Acute Respiratory Distress Syndrome (ARDS) Treatment-From Mice to Men.Biomedicines · 2022Review
- Simultaneous C5 and CD14 inhibition limits inflammation and organ dysfunction in pig polytrauma.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
Polymorphonuclear (PMN) leucocytes participate in acute inflammatory pathologies such as acute respiratory distress syndrome (ARDS) following traumatic injury and shock, which also activates the coagulation system systemically. Trauma can prime the PMN nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex for an enhanced respiratory burst, but the relative role of various priming agents in this process remains incompletely understood. We therefore set out to identify mediators of PMN priming during coagulation and trauma-shock and determine whether PMN reactive oxygen species (ROS) generated in this manner could influence organ injury and coagulation. Initial experiments demonstrated that PMN are primed for predominantly extracellular ROS production by products of coagulation, which was abrogated by CD88/C5a receptor(C5aR) inhibition. The importance of this was highlighted further by demonstrating that known PMN priming agents result in fractionally different amounts of extracellular versus intracellular ROS release depending on the agent used. Plasma from trauma patients in haemodynamic shock (n = 10) also primed PMN for extracellular ROS in a C5a-dependent manner, which correlated with both complement alternative pathway activation and thrombin generation. Furthermore, PMN primed by preincubation with products of blood coagulation directly caused loss of endothelial barrier function in vitro that was abrogated by C5aR blockade or NADPH oxidase inhibition. Finally, we show in a murine model of trauma-shock that p47phox knock-out (KO) mice with PMN incapable of generating ROS were protected from inflammatory end-organ injury and activated protein C-mediated coagulopathy. In summary, we demonstrate that trauma-shock and coagulation primes PMN for predominantly extracellular ROS production in a C5a-dependent manner that contributes to endothelial barrier loss and organ injury, and potentially enhances traumatic coagulopathy.
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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.