ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2008
Functions of the complement components C3 and C5 during sepsis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 80 citations in OpenAlex.
- C5aR1 and cGAS/STING and their possible involvement in radiosensitivity of colorectal cancer.iScience · 2026Review
- Complement levels and their diagnostic utility in neonatal sepsis.BMC pediatrics · 2025Article
- C3 as a predictive and prognostic biomarker in adult hemophagocytic lymphohistiocytosis: a large cohort study in China.Blood advances · 2025Article
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- C3-dependent effector functions of complement.Immunological reviews · 2023Review
- Oral microbiome mediated inflammation, a potential inductor of vascular diseases: a comprehensive review.Frontiers in cardiovascular medicine · 2023Review
- A system pharmacology Boolean network model for the TLR4-mediated inflammatory response in early sepsis.Journal of pharmacokinetics and pharmacodynamics · 2022Article
- Biomarkers for the Prediction and Judgement of Sepsis and Sepsis Complications: A Step towardsJournal of clinical medicine · 2022Review
- The Interplay between Host Defense, Infection, and Clinical Status in Septic Patients: A Narrative Review.International journal of molecular sciences · 2022Review
- Aspects of the Complement System in New Era of Xenotransplantation.Frontiers in immunology · 2022Review
- Complement as driver of systemic inflammation and organ failure in trauma, burn, and sepsis.Seminars in immunopathology · 2021Review
- Characterization and functional analysis of hybrid pearl gentian grouper (Fish and shellfish immunology reports · 2021Article
- Complement levels in patients with bloodstream infection due to Staphylococcus aureus or Gram-negative bacteria.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020Article
- Article
- Role of Complement and Histones in Sepsis.Frontiers in medicine · 2020Review
- Targeting Complement Pathways in Polytrauma- and Sepsis-Induced Multiple-Organ Dysfunction.Frontiers in immunology · 2019Review
- Cytokine Profile in Early Infection byJournal of immunology research · 2019Article
- Inhibition of complement C5 protects against organ failure and reduces mortality in a baboon model ofProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Activation of the complement cascade enhances motility of leukemic cells by downregulating expression of HO-1.Leukemia · 2017Article
- Lung Metabolic Activation as an Early Biomarker of Acute Respiratory Distress Syndrome and Local Gene Expression Heterogeneity.Anesthesiology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Activation of the complement system is a key event in the pathogenesis of sepsis. Nevertheless, the exact mechanisms remain inadequately understood. In the current study, we examined the role of complement C3 and C5 in sepsis in wild-type and C3- or C5-deficient mice induced by cecal ligation and puncture. When compared to wild-type mice, C5(-/-) showed identical survival, and C3(-/-) presented significantly reduced survival. Interestingly, this was associated with significant decreases in plasma levels of proinflammatory mediators. Moreover, although septic C3(-/-) animals displayed a 10-fold increase of blood-borne bacteria, C5(-/-) animals exhibited a 400-fold increase in bacteremia when compared to wild-type mice. These effects were linked to the inability of C5(-/-) mice to assemble the terminal membrane attack complex (MAC), as determined by complement hemolytic activity (CH-50). Surprisingly, although negative control C3(-/-) mice failed to generate the MAC, significant increases of MAC formation was found in septic C3(-/-) mice. In conclusion, our data corroborate that hemolytic complement activity is essential for control of bacteremia in septic mice. Thus, during sepsis, blockade of C5a or its receptors (rather than C5) seems a more promising strategy, because C5a-blockade still allows for MAC formation while the adverse effects of C5a are prevented.
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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.