ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
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.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 59 citations in OpenAlex.
- Targeting Microglial C5aR1 with PMX205 Attenuates Neuroinflammation and Improves Neurological Recovery After Intracerebral Hemorrhage.Neurochemical research · 2026Article
- The complement system: A key player in the host response to infections.European journal of immunology · 2024Review
- Early identification and diagnosis, pathophysiology, and treatment of sepsis-related acute lung injury: a narrative review.Journal of thoracic disease · 2024Review
- Africanized honeybee venom (Frontiers in immunology · 2024Article
- Disruption of the C5a/C5aR1 axis confers protection against hookworm infection in lung.Frontiers in immunology · 2024Article
- International expert consensus on diagnosis and treatment of lung cancer complicated by chronic obstructive pulmonary disease.Translational lung cancer research · 2023Review
- Complosome - the intracellular complement system.Nature reviews. Nephrology · 2023Review
- C5aR1 signaling triggers lung immunopathology in COVID-19 through neutrophil extracellular traps.The Journal of clinical investigation · 2023Article
- Immunomodulation of neutrophil granulocyte functions by bacterial polyphosphates.European journal of immunology · 2023Article
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- New Insights into the Role of the Complement System in Human Viral Diseases.Biomolecules · 2022Review
- In Vivo Pharmacodynamic Method to Assess Complement C5a Receptor Antagonist Efficacy.ACS pharmacology & translational science · 2022Article
- Bacterial polyphosphates induce CXCL4 and synergize with complement anaphylatoxin C5a in lung injury.Frontiers in immunology · 2022Article
- FJU-C28 inhibits the endotoxin-induced pro-inflammatory cytokines expression via suppressing JNK, p38 MAPK and NF-κB signaling pathways.Pharmacology research & perspectives · 2021Article
- Intrabronchial application of extracellular histones shows no proinflammatory effects in swine in a translational pilot study.BMC research notes · 2021Article
- CCR5 Antagonist Maraviroc Inhibits Acute Exacerbation of Lung Inflammation Triggered by Influenza Virus in Cigarette Smoke-Exposed Mice.Pharmaceuticals (Basel, Switzerland) · 2021Article
- C5a-C5aR1 Axis Activation Drives Envenomation Immunopathology by the SnakeFrontiers in immunology · 2021Article
- Persistence of High Levels of Serum Complement C5a in Severe COVID-19 Cases After Hospital Discharge.Frontiers in immunology · 2021Article
- Article
- The Complement C5a-C5aR1 GPCR Axis in COVID-19 Therapeutics.Trends in immunology · 2020Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Excessive activation of the complement system is detrimental in acute inflammatory disorders. In this study, we analyzed the role of complement-derived anaphylatoxins in the pathogenesis of experimental acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in C57BL/6J mice. Intratracheal administration of recombinant mouse complement component (C5a) caused alveolar inflammation with abundant recruitment of Ly6-G(+)CD11b(+) leukocytes to the alveolar spaces and severe alveolar-capillary barrier dysfunction (C5a-ALI; EC(50[C5a]) = 20 ng/g body weight). Equimolar concentrations of C3a or desarginated C5a (C5a(desArg)) did not induce alveolar inflammation. The severity of C5a-ALI was aggravated in C5-deficient mice. Depletion of Ly6-G(+) cells and use of C5aR1(-/-) bone marrow chimeras suggested an essential role of C5aR1(+) hematopoietic cells in C5a-ALI. Blockade of PI3K/Akt and MEK1/2 kinase pathways completely abrogated lung injury. The mechanistic description is that C5a altered the alveolar cytokine milieu and caused significant release of CC-chemokines. Mice with genetic deficiency of CC-chemokine receptor (CCR) type 5, the common receptor of chemokine (C-C motif) ligand (CCL) 3, CCL4, and CCL5, displayed reduced lung damage. Moreover, treatment with a CCR5 antagonist, maraviroc, was protective against C5a-ALI. In summary, our results suggest that the detrimental effects of C5a in this model are partly mediated through CCR5 activation downstream of C5aR1, which may be evaluated for potential therapeutic exploitation in ALI/ARDS.
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