ArticleThe Journal of clinical investigation1996
Requirement and role of C5a in acute lung inflammatory injury in rats.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 200 citations in OpenAlex.
- Inadequate cytoplasmatic calcium signals in alveolar macrophages after cardiac surgery.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2010Trial
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- An anti-complement homogeneous polysaccharide fromActa pharmaceutica Sinica. B · 2025Article
- Complement System and Adhesion Molecule Skirmishes in Fabry Disease: Insights into Pathogenesis and Disease Mechanisms.International journal of molecular sciences · 2024Review
- Complement system activation: bridging physiology, pathophysiology, and therapy.Intensive care medicine · 2024Review
- Treatment with Cobra Venom Factor Decreases Ischemic Tissue Damage in Mice.Biomedicines · 2024Article
- The complement cascade in lung injury and disease.Respiratory research · 2024Review
- C5aR1 signaling triggers lung immunopathology in COVID-19 through neutrophil extracellular traps.The Journal of clinical investigation · 2023Article
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Bacterial polyphosphates induce CXCL4 and synergize with complement anaphylatoxin C5a in lung injury.Frontiers in immunology · 2022Article
- Plant polysaccharides with anti-lung injury effects as a potential therapeutic strategy for COVID-19.Frontiers in pharmacology · 2022Review
- Pretreatment with atorvastatin ameliorates cobra venom factor-induced acute lung inflammation in mice.BMC pulmonary medicine · 2020Article
- Complement Inhibition in Severe COVID-19 Acute Respiratory Distress Syndrome.Frontiers in pediatrics · 2020Article
- Review
- Blood clotting and traumatic injury with shock mediates complement-dependent neutrophil priming for extracellular ROS, ROS-dependent organ injury and coagulopathy.Clinical and experimental immunology · 2018Article
- Beneficial effects ofActa pharmaceutica Sinica. B · 2018Article
- C5L2, the Second C5a Anaphylatoxin Receptor, Suppresses LPS-Induced Acute Lung Injury.American journal of respiratory cell and molecular biology · 2016Article
- New Insights into Molecular Mechanisms of Immune Complex-Induced Injury in Lung.Frontiers in immunology · 2016Review
- Experimental design of complement component 5a-induced acute lung injury (C5a-ALI): a role of CC-chemokine receptor type 5 during immune activation by anaphylatoxin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
9 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
11 authors at 5 institutions in 5 countries.
Funding
Abstract
The complement activation product, C5a, may play a key role in the acute inflammatory response. Polyclonal antibody to rat C5a was used to define the requirements for C5a in neutrophil-dependent inflammatory lung injury after systemic activation of complement by cobra venom factor (CVF) or after intrapulmonary deposition of IgG immune complexes. In the CVF model, intravenous infusion (but not intratracheal instillation) of anti-C5a produced a dose-dependent reduction in lung permeability and in lung content of myeloperoxidase. In C6-deficient rats, CVF infusion caused the same level of lung injury (measured by leak of 125I-albumin) as found in C6-sufficient rats. In the IgG immune complex model of lung injury, anti-C5a administered intratracheally (but not intravenously) reduced in a dose-dependent manner both the increase in lung vascular permeability as well as the buildup of lung myeloperoxidase. Treatment with anti-C5a greatly suppressed upregulation of lung vascular intercellular adhesion molecule-1 (ICAM-1). This was correlated with a substantial drop in levels of TNFalpha in bronchoalveolar fluids. These data demonstrate the requirement for C5a in the two models of injury. In the IgG immune complex model, C5a is required for the full production of TNFalpha and the corresponding upregulation of lung vascular ICAM-1.
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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.