ArticleInfection and immunity1999
Complement-dependent accumulation and degradation of platelets in the lung and liver induced by injection of lipopolysaccharides.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 71 citations in OpenAlex.
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- Signaling pathways and intervention therapies in sepsis.Signal transduction and targeted therapy · 2021Review
- The Toxicology of Native Fucosylated Glycosaminoglycans and the Safety of Their Depolymerized Products as Anticoagulants.Marine drugs · 2021Article
- [Rituximab-induced acute thrombocytopenia in a patient with splenic marginal zone lymphoma: a case report and literature review].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2021Review
- The role of platelets in sepsis.Research and practice in thrombosis and haemostasis · 2021Article
- The role of O-polysaccharide chain and complement resistance of Escherichia coli in mammary virulence.Veterinary research · 2020Article
- Platelets in Sepsis: An Update on Experimental Models and Clinical Data.Frontiers in immunology · 2019Review
- Impact of Escherichia coli K12 and O18:K1 on human platelets: Differential effects on platelet activation, RNAs and proteins.Scientific reports · 2018Article
- Rituximab-induced Acute Thrombocytopenia in Granulomatosis with Polyangiitis.Internal medicine (Tokyo, Japan) · 2018Article
- Interaction of Mannose-Binding Lectin With Lipopolysaccharide Outer Core Region and Its Biological Consequences.Frontiers in immunology · 2018Article
- Genetically regulated hepatic transcripts and pathways orchestrate haematological, biochemical and body composition traits.Scientific reports · 2016Article
- Platelets in Pulmonary Immune Responses and Inflammatory Lung Diseases.Physiological reviews · 2016Review
- Blockade of Thrombopoietin Reduces Organ Damage in Experimental Endotoxemia and Polymicrobial Sepsis.PloS one · 2016Article
- Role for platelet glycoprotein Ib-IX and effects of its inhibition in endotoxemia-induced thrombosis, thrombocytopenia, and mortality.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Platelets as cellular effectors of inflammation in vascular diseases.Circulation research · 2013Review
- Platelets induce apoptosis during sepsis in a contact-dependent manner that is inhibited by GPIIb/IIIa blockade.PloS one · 2012Article
- Lipopolysaccharide signaling without a nucleus: kinase cascades stimulate platelet shedding of proinflammatory IL-1β-rich microparticles.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Lipopolysaccharide stimulates platelet secretion and potentiates platelet aggregation via TLR4/MyD88 and the cGMP-dependent protein kinase pathway.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Caecal ligation and puncture in the rat mimics the pathophysiological changes in human sepsis and causes multi-organ dysfunction.Metabolic brain disease · 2007Article
- Critical roles of platelets in lipopolysaccharide-induced lethality: effects of glycyrrhizin and possible strategy for acute respiratory distress syndrome.International immunopharmacology · 2005Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We found unique behaviors among platelets within a few minutes of the intravenous injection of lipopolysaccharide (LPS) into mice. Platelets accumulated primarily in the liver at lower doses of LPS, but at higher doses they accumulated largely in the lungs. When the platelets accumulated in these organs were degraded, there was a rapid anaphylactoid shock. The platelet response depended on the strain of mouse and on the source of LPS. Of various LPSs tested, the LPS from the smooth type of Klebsiella O3 (KO3-S LPS) was the most potent at inducing the platelet response and shock. K-76 monocarboxylic acid, an inhibitor of complement C5, effectively prevented the KO3-S LPS-induced degradation (but not accumulation) of platelets and the ensuing rapid shock in BALB/c mice. Moreover, in DBA/2 mice (which are deficient in complement C5), platelets accumulated in the lungs and liver in response to KO3-S LPS but soon returned to the circulation without degradation, and there was no rapid shock. The LPS from the rough type of KO3 induced an accumulation of platelets in the liver and lungs but not a degradation of platelets. On the basis of these results and those reported by other investigators, we propose that in the platelet response to LPS, the lectin pathway to form C3 convertase from C4 and C2 is involved in the rapid accumulation of platelets in the liver and lungs and that the pathway from C5 to C9 is involved in the destruction of platelets and the consequent anaphylactoid shock.
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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.