ArticleThe Journal of clinical investigation2000
Protective effects of anti-C5a in sepsis-induced thymocyte apoptosis.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
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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
47 citing papers in PubMed, 156 citations in OpenAlex.
- Post-ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat.Physiological reports · 2025Article
- 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
- Complement Factor C5a Inhibits Apoptosis of Neutrophils-A Mechanism in Polytrauma?Journal of clinical medicine · 2021Article
- Article
- Role of complement C5a and histones in septic cardiomyopathy.Molecular immunology · 2018Review
- Mechanism of C5a-induced immunologic derangement in sepsis.Cellular & molecular immunology · 2017Article
- Complement C5a induces mesenchymal stem cell apoptosis during the progression of chronic diabetic complications.Diabetologia · 2017Article
- Complement and sepsis-induced heart dysfunction.Molecular immunology · 2017Review
- Role of Complement C5 in Experimental Blunt Chest Trauma-Induced Septic Acute Lung Injury (ALI).PloS one · 2016Article
- Temporal Progression of Pneumonic Plague in Blood of Nonhuman Primate: A Transcriptomic Analysis.PloS one · 2016Article
- Complement 5a receptor-mediated neutrophil dysfunction is associated with a poor outcome in sepsis.Cellular & molecular immunology · 2016Article
- Protein kinase C-δ mediates sepsis-induced activation of complement 5a and urokinase-type plasminogen activator signaling in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Complement in animal development: unexpected roles of a highly conserved pathway.Seminars in immunology · 2013Review
- Article
- New insights for C5a and C5a receptors in sepsis.Frontiers in immunology · 2012Article
- Manipulation of the complement system for benefit in sepsis.Critical care research and practice · 2012Article
- Molecular mechanisms of inflammation and tissue injury after major trauma--is complement the "bad guy"?Journal of biomedical science · 2011Review
- Ecto-5'-nucleotidase (CD73) decreases mortality and organ injury in sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- γδT-cell function in sepsis is modulated by C5a receptor signalling.Immunology · 2011Article
- Complement activation in emergency department patients with severe sepsis.Academic emergency medicine : official journal of the Society for Academic Emergency Medicine · 2010Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
Abstract
Multiorgan apoptosis occurs during sepsis. Following cecal ligation and puncture (CLP) in rats, thymocytes underwent apoptosis in a time-dependent manner. C5a blockade dramatically reduced thymocyte apoptosis as measured by thymic weight, binding of annexin V to thymocytes, and laddering of thymocyte DNA. When C5a was generated in vivo by infusion of purified cobra venom factor (CVF), thymocyte apoptosis was significantly increased. Similar results were found when CVF was injected in vivo during the early stages of CLP. In animals 12 hours after induction of CLP, there was an increase in the activities of caspase-3, -6, and -9, but not caspase-1 and -8. Cytosolic cytochrome c levels increased by twofold, whereas mitochondrial levels showed a 50% decrease. Western blot analysis revealed that the content of Bcl-X(L) (but not of Bcl-2, BAX, Bad, and Bim) significantly decreased in thymocytes after CLP. C5a blockade in the sepsis model almost completely inhibited caspase-3, -6, and -9 activation, significantly preserved cytochrome c in the mitochondrial fraction, and restored Bcl-X(L) expression. These data suggest that systemic activation of complement induces C5a-dependent apoptosis of thymocytes and that the blockade of C5a during sepsis rescues thymocytes from apoptosis.
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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.