ArticleCritical care (London, England)2010
Activated protein C ameliorates coagulopathy but does not influence outcome in lethal H1N1 influenza: a controlled laboratory study.
Article in Critical care (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
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- Decoding Sepsis-Induced Disseminated Intravascular Coagulation: A Comprehensive Review of Existing and Emerging Therapies.Journal of clinical medicine · 2023Review
- Application of weighted gene co-expression network analysis to identify the hub genes in H1N1.International journal of physiology, pathophysiology and pharmacology · 2021Article
- Oral Fucoidan Attenuates Lung Pathology and Clinical Signs in a Severe Influenza a Mouse Model.Marine drugs · 2020Article
- iTRAQ-based quantitative proteomics reveals important host factors involved in the high pathogenicity of the H5N1 avian influenza virus in mice.Medical microbiology and immunology · 2017Article
- Anticoagulation increases alveolar hemorrhage in mice infected with influenza A.Physiological reports · 2016Article
- Aberrant coagulation causes a hyper-inflammatory response in severe influenza pneumonia.Cellular & molecular immunology · 2016Review
- Tissue factor deficiency increases alveolar hemorrhage and death in influenza A virus-infected mice.Journal of thrombosis and haemostasis : JTH · 2016Article
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- Switch from protective to adverse inflammation during influenza: viral determinants and hemostasis are caught as culprits.Cellular and molecular life sciences : CMLS · 2014Review
- PAR-1 contributes to the innate immune response during viral infection.The Journal of clinical investigation · 2013Article
- Protease-activated receptor-1 impairs host defense in murine pneumococcal pneumonia: a controlled laboratory study.Critical care (London, England) · 2012Article
- Review: Viral infections and mechanisms of thrombosis and bleeding.Journal of medical virology · 2012Review
- Report of the 'mechanisms of lung injury and immunomodulator interventions in influenza' workshop, 21 March 2010, Ventura, California, USA.Influenza and other respiratory viruses · 2011Article
- Genomic profiling of tumor necrosis factor alpha (TNF-alpha) receptor and interleukin-1 receptor knockout mice reveals a link between TNF-alpha signaling and increased severity of 1918 pandemic influenza virus infection.Journal of virology · 2010Article
- Activated protein C for H1N1 influenza? More work to do!Critical care (London, England) · 2010Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionInfluenza accounts for 5 to 10% of community-acquired pneumonias and is a major cause of mortality. Sterile and bacterial lung injuries are associated with procoagulant and inflammatory derangements in the lungs. Activated protein C (APC) is an anticoagulant with anti-inflammatory properties that exert beneficial effects in models of lung injury. We determined the impact of lethal influenza A (H1N1) infection on systemic and pulmonary coagulation and inflammation, and the effect of recombinant mouse (rm-) APC here on.
methodsMale C57BL/6 mice were intranasally infected with a lethal dose of a mouse adapted influenza A (H1N1) strain. Treatment with rm-APC (125 microg intraperitoneally every eight hours for a maximum of three days) or vehicle was initiated 24 hours after infection. Mice were euthanized 48 or 96 hours after infection, or observed for up to nine days.
resultsLethal H1N1 influenza resulted in systemic and pulmonary activation of coagulation, as reflected by elevated plasma and lung levels of thrombin-antithrombin complexes and fibrin degradation products. These procoagulant changes were accompanied by inhibition of the fibrinolytic response due to enhanced release of plasminogen activator inhibitor type-1. Rm-APC strongly inhibited coagulation activation in both plasma and lungs, and partially reversed the inhibition of fibrinolysis. Rm-APC temporarily reduced pulmonary viral loads, but did not impact on lung inflammation or survival.
conclusionsLethal influenza induces procoagulant and antifibrinolytic changes in the lung which can be partially prevented by rm-APC treatment.
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