ArticleThe Journal of clinical investigation2002
Increased C5a receptor expression in sepsis.
Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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.
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
85 citing papers in PubMed, 193 citations in OpenAlex.
- Pre-existing antibody-mediated adverse effects prevent the clinical development of a bacterial anti-inflammatory protein.Disease models & mechanisms · 2020Trial
- Plasma C5a and serum C5aR levels in patients with chronic spontaneous urticaria: A single-center case-control study.PloS one · 2026Article
- Article
- The immunology of sepsis: translating new insights into clinical practice.Nature reviews. Nephrology · 2026Review
- 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
- Combatting sepsis-induced myocardial dysfunction: emerging mechanisms and immunomodulatory breakthroughs.Frontiers in immunology · 2025Review
- Pathophysiological dynamics in the contact, coagulation, and complement systems during sepsis: Potential targets for nafamostat mesilate.Journal of intensive medicine · 2024Review
- Identification of a genetic region linked to tolerance to MRSA infection using Collaborative Cross mice.PLoS genetics · 2024Article
- Africanized honeybee venom (Frontiers in immunology · 2024Article
- FBXO11 governs macrophage cell death and inflammation in response to bacterial toxins.Life science alliance · 2023Article
- Inflammatory mechanisms and intervention strategies for sepsis-induced myocardial dysfunction.Immunity, inflammation and disease · 2023Review
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- 3'mRNA sequencing reveals pro-regenerative properties of c5ar1 during resolution of murine acetaminophen-induced liver injury.NPJ Regenerative medicine · 2022Article
- Complement Regulation in Human Tenocytes under the Influence of Anaphylatoxin C5a.International journal of molecular sciences · 2021Article
- Role of the C5a-C5a receptor axis in the inflammatory responses of the lungs after experimental polytrauma and hemorrhagic shock.Scientific reports · 2021Article
- Targeting Complement C5a Receptor 1 for the Treatment of Immunosuppression in Sepsis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Article
- Sepsis therapies: learning from 30 years of failure of translational research to propose new leads.EMBO molecular medicine · 2020Review
- Role of Complement and Histones in Sepsis.Frontiers in medicine · 2020Review
- Distinct roles of the anaphylatoxin receptors C3aR, C5aR1 and C5aR2 in experimental meningococcal infections.Virulence · 2019Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Excessive production of the complement activation product C5a appears to be harmful during the development of sepsis in rodents. Little is known about the role of the C5a receptor (C5aR) and its presence in different organs during sepsis. Using the cecal ligation/puncture (CLP) model in mice, we show here that C5aR immunoreactivity was strikingly increased in lung, liver, kidney, and heart early in sepsis in both control and neutrophil-depleted mice. C5aR mRNA expression in these organs was also significantly increased during sepsis. Immunohistochemical analysis revealed patterns of increased C5aR expression in parenchymal cells in all four organs following CLP. Mice injected at the start of CLP with a blocking IgG to C5aR (alphaC5aR) showed dramatically improved survival when compared with animals receiving nonspecific IgG, as did mice injected with alphaC5a. In alphaC5aR-treated mice, serum levels of IL-6 and TNF-alpha and bacterial counts in various organs were significantly reduced during CLP when compared with control CLP animals. These studies demonstrate for the first time that C5aR is upregulated in lung, liver, kidney, and heart during the early phases of sepsis and that blockade of C5aR is highly protective from the lethal outcome of sepsis.
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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.